MRCP PART 2 WRITTEN APRIL 2011 (recall of questions)

Discussion in 'MRCP Forum' started by Guest, Apr 7, 2011.

  1. Dr albarwari

    Dr albarwari Guest

    Yes Dr Hopeful even 50 BOF / day may not be enough time if you want to study all 3 sources,,,but I was intending pastest

    Kumar Mongar
    drabdulkhalik @ yahoo dot com
  2. i passsssssssssssssed
    dear barawari can you give me your contact e.mail
  3. am appearing for november 2011

    any body wud like to join and do discussions

    my mail--silentdoctor18 at yahoo dot com
  4. Kumar Mongar

    Kumar Mongar Guest

    Thank you for Dr Hopeful & Dr Albarwari for your kind support. Most of our forum friends are passed the exam and only a few are failed, I noticed only 3 persons who acknowledge fail the exam. Miss you guys and congratulation. I feel sad and I need to try again.
    Kumar
  5. kumar mongar

    i understand the as i was also in the same boat
  6. Dr Hopeful

    Dr Hopeful Guest

    Dr Kumar

    I am sure many who failed are keeping silent. Atleast you are brave and declaring it . Dont lose heart and go for JULY . How much score you had ?
  7. failed  doc

    failed doc Guest

    dear barawri can you please send for me your notes

    for each system I did my own notes "I made a word file for each system" and copied the important notes regarding each BOF from the explanation and paste it in the file I made "this is very important to do as I shall comment on it

    i would be very thankful fot your help god bless you
    and help you in paces my e mail
    sak77772004 at yahool com
  8. DR ALBARWARI

    PLEASE SEND TO ME ALSO PLEASE ALBARWARI BHAI


    for each system I did my own notes "I made a word file for each system" and copied the important notes regarding each BOF from the explanation and paste it in the file I made "this is very important to do as I shall comment on it
  9. Guest

    Guest Guest

    NOV 2011

    Dr Albarwari
    Congratulations
    Can you send to me also these notes
    Thankyou in advance
    E-mail
    dralraziegypt59@hotmail.com[/color
  10. Dr Hopeful

    Dr Hopeful Guest

    now I shall not remain behind :)

    Please send it to wobbler007 at aol.co.uk as well :D
  11. Guest

    Guest Guest

  12. OKO

    OKO Guest

    Dr Barwari

    Can you send me your notes Please

    FindingHimo at Gmai
  13. Dr albarwari

    Dr albarwari Guest

    CARDIOLOGY


    Endotracheal administration of drugs is no longer recommended
    • In PPCM,,, Heparin given even before carvedilol
    • In acute MI presented with cardiogenic shock we can give IV dopamine
    • Ventilator-associated pneumonia. It occurs 48-72 h after admission, and worsening pulmonary infiltrates despite negative fluid balance are suggestive of chest infection. Appropriate management is
    o fluid resuscitation to achieve optimal left heart filling pressure, and
    o intravenous antibiotics.
    o Inotropic support in the form of alpha agonist is indicated if fluid resuscitation alone does not improve the blood pressure.
    • Post inferior MI complete HB
    o If asymptomatic need NO treatment
    o If asymptomatic give atropine if no response to atropine we can do temporary pacemaker
    • Bradycardia,,,The 2010 UK resuscitation guidelines suggest using theophylline as a slow intravenous infusion (100 mg-200 mg).
    • Bradycardia-induced syncope
    o Admit and arrange a 24 hour tape as an inpatient
    o if cardiovascularly stable no need for atropin
    • Asystolic cardiac arrests updated 2010 UK resuscitation guidelines no longer recommend atropine for asystole Adrenaline alone - repeated doses every 3 to 5 minutes Isoprenaline has no role in asystolic cardiac arrests
    • Mobitz type II block in anterior myocardial infarction treated by temporary transvenous pacing regardless of symptoms "not option for Atropin"
    • Indications for transvenous pacing in acute MI are:
    o asystole
    o symptomatic sinus bradycardia or Mobitz I block not responding to atropine
    o Mobitz type II block in anterior myocardial infarction
    o Junctional escape rhythm + wide QRS
    o new bundle branch block (BBB) with first-degree heart block
    o an old right BBB with first degree atrioventricular (AV) block and a new fascicular block
    • Syncope + RBBB + left posterior fascicular block + PR interval is 190 ms,,,,here do not go directly for permanent pacemaker but Admit for 24 hours and follow up with 72hr - 1 week holter monitoring for possible episodes of complete heart block then if CHB present you can do pacemaker
    • When a monitored patient develops VF, and resuscitation and defibrillation equipment is closely available (as would be the case on CCU) the recommendation is to attach the defibrillator and administer a shock without delay "not do Praecordial thump"
    • Praecordial thump is only recommended if a patient has a witnessed arrest, is not monitored and/or immediate defibrillation is not available (and it should not delay calling for help or getting a defibrillator).
    • WPW syndrome with "narrow complex" presented with palpitation not respond to adenosine next step give either IV flecainide or disopyramide " Amiodarone less effective in cardioversion"
    • WPW syndrome + AF "broad complex" best treatment is IV Flecainide
    • AF + Heart failure can be treated with Digoxin or b-blocker
    • Paroxysmal AF + mild Left venyricular impairment best treatment is bisoprolol + warfarin
    • Paroxysmal AF + normal heart need cardioversion best treatment is flecainide + LMWH
    • AF + normal heart need cardioversion best treatment is flecainide which is better than sotalol
    • Patient presented with acute onset AF. The immediate need would be to rate control his atrial fibrillation and try and manage chemical cardioversion WITH anticoagulation "eg Amiodarone + LMWH"
    • Patient with congestive heart failure and AF the best drug to stabilise the patient cardiovascularly before the imminent surgery is Amiodarone not Esmolol
    • Patient with Mitral valve stenosis "not in failure" + AF the best drug to stabilise the patient is IV Esmolol
    • Paroxysmal SVT,, best treatment is adenosine then verapamil then sotalol
    • Patient with an acute coronary syndrome and rapid narrow complex tachycardia ,,,Give her a fast intravenous (IV) dose of adenosine 6 mg and repeating it if there is no response "not give b blocker'
    • Atrial flutter
    o Radiofrequency ablation of typical AFL has a long-term success rate of greater than 90%
    o Flecainide should not be used as a single agent
    o Flecainide may be used in conjunction with AV nodal blocking agents, such as a β-blocker or a nondihydropyridine calcium channel blocker
    • The treatment for polymorphic ventricular tachycardia is
    o synchronised cardioversion when the patient is unstable
    o magnesium and potassium to correct any electrolyte imbalances and overdrive pacing.
    • Stent thrombosis usually occurs in the first two days after the procedure presented with myocardial infarction treatment by Intravenous (IV) abciximab and immediate transfer to Cardiac Catheterisation L for intracoronary thrombolytic therapy
    • In pulseless ventricular tachycardia the initial shock should be 360 J unsynchronized
    • VT has RBBB pattern while SVT + aberrant conduction has LBBB pattern
    • Verapamil is preferred on Amiodarone for SVT cardioversion
    • Patients with prosthetic valve subacute bacterial endocarditis (usually with viridans Streptococci) often have minmal symptoms and there may be NO fever
    • Patient with mycoplasma pneumonia on Amitryptilin give him Doxycyclin "not Erythromycin" because of QT interval prolongation
    • Flash pulmonary oedema. The most common cause is
    o Myocardial ischaemia."ECG changes"
    o Bilateral renal artery stenosis "less common"
    • Post MI cardiogenic shock
    o Dopamine is CI
    o IABP "ballon pump" is indicated
    • Dyspnea in HOCM
    o b-blockade first choice
    o but if the outflow gradient is greater than 50 mmHg, surgical myomectomy is usually recommended. Unfortunately surgery does not reduce the risk of arrhythmia
    • 750 ml bottle of 12% wine contains nine units alcohol,,,more than 50 units alcohol is excess and need to be reduced in patient with hypertension
    • Treatment of overweight, diabetic patients with metformin, lowers the relative risk of myocardial infarction (MI) by 40%, as opposed to treatment with sulphonylureas or insulin
    • There is no evidence that commencing T2Ds on insulin lowers the risk of MI, even if the HbA1c improves
    • The presence of a VSD would be confirmed by detecting a step-up in the oxygen saturation between the RA and PA; if there is no step-up, the diagnosis is probably papillary muscle rupture
  14. Dr albarwari

    Dr albarwari Guest

    CARDIOLOGY


    Trifascicular block is a term used for the combination of
     right bundle branch block,
     left hemiblock (typically left anterior hemiblock) and
     long PR interval
    o Clinically it means there is extensive disease of the conduction system and, in a patient such as this, would be an indication for permanent pacemaker





    Indications for permanent pacemaker implantation include
    • third-degree block,
    • symptomatic Wenckebach phenomenon,
    • asymptomatic type II second-degree block, and
    • pauses of >3.0 s.
    • Symptomatic sinus node dysfunction is an indication for pacemaker placement, even if the bradycardia occurs as a consequence of drug therapy, if there is no acceptable alternative.
    Type 2 second degree block
    • most often occurs in the His-Purkinje system; as such this poses a higher risk to the patient of progression to complete heart block.
    • syncopal attacks. Optimal management is therefore referral for permanent pacing.

    Pacemaker syndrome
    • Occur in VVI
    • An untimely contraction of the atria caused by retrograde conduction of the ventricular pacemaker impulse mimics complete heart block and the pounding is the feeling of atria contracting against a closed tricuspid valve causing cannon waves in the neck.
    • The treatment is to upgrade the system to a dual chamber pacemaker; this allows the atria to sense any retrograde electrical impulse, so inhibiting native atrial depolarisation.

    Lead displacement in pacemaker implantation.
    • The lead can displace through the ventricle into the pericardial space, leading to pain with features suggestive of pericarditis.
    • Electrical stimulation of the diaphragm may be experienced as hiccoughs.
    • A chest X-ray would reveal the displaced lead in most cases.

    Sick sinus syndrome, cause episodes of bradycardia and tachycardia. Anti-arrhythmics are likely to exacerbate any bradycardia and the treatment of choice would be a permanent pacemaker. Dual chamber pacemakers are usually used, as single chamber pacing may be associated with the development of ‘pacemaker syndrome’.
    Paroxysmal atrial fibrillation + complete heart block + ejection fraction points towards impairment of LV function. Management of choice in this case is dual chamber pacing, She should continue her sotalol to prevent further episodes of atrial fibrillation.

    AV Block after inferior MI
    • no prognostic significance
    • usually resolves in the first 24 h.
    • If the patient is haemodynamically stable and asymptomatic, should continue to be monitored
    • If symptomatic give atropin

    Indications for permanent pacemaker implantation include
    • third-degree heart block,
    • symptomatic second-degree block,
    • asymptomatic type II second-degree block
    • pauses of more than 3.0 s.

    Carotid sinus hypersensitivity
    • exaggerated response to carotid sinus stimulation.
    • The diagnosis is only made after ischaemic heart disease or rhythm disturbance have been reasonably excluded, as in this case.
    • CSH may be
    o predominantly cardioinhibitory (resulting in bradycardia),
    o vasodilatory (resulting in hypotension),
    o or a mixture of the two.
    • Cardioinhibitory CSH is usually managed with insertion of a dual-chamber pacemaker, and
    • vasodilatory CSH is managed with support stockings, fludrocortisone and midodrine




    • Do not give atropine to patients with cardiac transplants. Their hearts are denervated and will not respond to vagal blockade by atropine, which may cause paradoxical sinus arrest or high-grade AV block in these patients
    • If bradycardia with adverse signs persist despite atropine, consider cardiac pacing. If pacing cannot be achieved promptly consider the use of second-line drugs
    • consider giving intravenous glucagon if a beta-blocker or calcium channel blocker is a likely cause of the bradycardia
    • Consider using theophylline (100-200 mg by slow intravenous injection) for bradycardia complicating
    • acute inferior wall myocardial infarction,
    • spinal cord injury or
    • cardiac transplantation

    In structurally normal heart with Paroxysmal SVT
    • Sotalol, a class III anti-arrhythmic agent would probably represent the best choice of the options given for this man.
    • An alternative would be a class 1c agent such as flecainide where patients suffer side-effects such as erectile dysfunction on β-blockade or verapamil.

    Recurrent atrial flutter (AFL)
    • “Typical†AFL is a macroreentrant circuit that rotates counter-clockwise around the tricuspid valve
    • Radiofrequency ablation of typical AFL has a long-term success rate of greater than 90%
    • Flecainide should not be used as a single agent in patients with AFL. It can enhance AV nodal conduction, which may cause 1:1 transmission of AFL waves and result in ventricular fibrillation.
    • Flecainide may be used in conjunction with AV nodal blocking agents, such as a β-blocker or a nondihydropyridine calcium channel blocker.


    VT Treatment
    • If compromised with a low blood pressure, even though asymptomatic, the treatment of choice is DC cardioversion.
    • In pulseless ventricular tachycardia the initial shock should be 360 J unsynchronised. The rationale for using unsynchronised shock in pulseless VT is to avoid the slight delay that might occur with synchronised shock.
    • Pulseless VT has the same protocol as ventricular fibrillation.
    In a witnessed VF arrest the guidelines now suggest that
    • a single DC shock is given (either a single biphasic (150–360 J) or monophasic (360 J) shock) followed by immediate chest compressions (without feeling for a pulse or reassessing rhythm).
    • After 2 min of CPR the rhythm should be reassessed and if still VF a further DC shock should be given. monophasic (360 J)
    • After a further 2 min of CPR of VF persist iv adrenaline should be given followed by a further DC shock.
    appropriate energy on the defibrillator (150-200 J biphasic for the first shock and 150-360 J biphasic for subsequent shocks)
    Despite the fact if there is acidosis, the use of sodium bicarbonate is no longer recommended as part of the ALS algorithm drawn up by the UK resuscitation council. It may however still be considered in cases of profound hyperkalaemia or where there is overdose of tricyclic antidepressants.
    Amiodarone 300mg IV is part of the guidelines for the treatment of persistent VF/VT (with pulse) after three shocks have been given.
    Where there is suspicion of hypovolaemia, e.g. after massive blood loss due to trauma, then IV fluids may be of value.
    At core temperatures of less than 30°C, treatment of ventricular arrhythmias with medical therapy is largely ineffective and electrical cardioversion is less effective. For this reason, a prolonged period of CPR may be required until core temperature is above 30ºC. Where available, for a long period of cardiac arrest, cardiopulmonary bypass may be effective, although practically this would be possible in only a handful of centres within the UK. Recovery is usually complete for patients with mild to moderate hypothermia (28ºC or higher core temperature) and no pre-existing medical conditions,
    severe hypothermia coupled with pre-existing medical illness carries a mortality of around 50%.

    Precordial thump
    • A single precordial thump has a very low success rate for cardioversion of a shockable rhythm and is only likely to succeed if given within the first few seconds of the onset of a shockable rhythm.
    • There is more success with pulseless VT than with VF.
    • Delivery of a precordial thump must not delay calling for help or accessing a defibrillator.
    • It is therefore appropriate therapy only when several clinicians are present at a witnessed, monitored arrest, and when a defibrillator is not immediately to hand. In practice, this is likely to be in a monitored environment such as the emergency department resuscitation room, ICU, CCU, cardiac catheter laboratory or pacemaker room.

    Torsade de pointes
    haemodynamically unstable should be treated with electrical cardioversion.
    If stable
    Magnesium and potassium are first-line
    Other therapies include overdrive pacing and
    isoproterenol infusion.
    supraventricular tachycardia (SVT) + Asthma
    • Adenosine is contraindicated in asthmatic patients as is beta-blockade with labetolol.
    • The safest alternatives would be IV verapamil or iv flecainide in this patient
    Vagal manoeuvres or adenosine will terminate almost all AVNRT or AVRT within seconds. Failure to terminate a regular narrow-complex tachycardia with adenosine suggests an atrial tachycardia such as atrial flutter (unless the adenosine has been injected too slowly or into a small peripheral vein).




    Wolff Parkinson White (WPW) syndrome.
    • If the tachycardia has a narrow QRS complex the anterograde limb (the pathway that conducts impulse to ventricle) is the atrioventricular (AV) node, while the retrograde limb is the accessory pathway.
    1. The delta wave in this case is lost.
    2. This type of tachycardia is called orthodromic AV re-entrant tachycardia. Termination of orthodromic AV re-entrant tachycardia involves
     manoeuvres that depress conduction through the AV node such as carotid sinus massage or a Valsalva manoeuvre;
     if not successful then drugs that depress AV nodal conduction like adenosine is used.
     Digoxin and verapamil should be avoided as they may accelerate conduction down the accessory pathway.
     Intravenous flecainide or disopyramide should be used for chemical cardioversion. Beta-blockers may also be used.
     Amiodarone is slightly less effective in achieving cardioversion in this situation than flecainide.
     DC cardioversion should be used early if the tachycardia is causing haemodynamic comprise.
     If symptoms are recurrent, patients should be referred for Radio-frequency ablation, which is the definitive treatment.
    Atrial fibrillation of Acute onset
    • The immediate need would be to rate control his atrial fibrillation and try and manage chemical cardioversion, in which case IV amodarone is an obvious choice.
    • Digoxin would not encourage reversion to sinus rhythm so would not be the first choice here.
    • The likely outcome is the patient reverting back to sinus rhythm within hours.
    • If the patient does not revert back to sinus rhythm, formal anticoagulation would need to be instituted.
    • He would also need to be investigated for the cause of the atrial fibrillation.
    • Electrical cardioversion may be an option post anti-coagulation and may still be considered acutely if he remains compromised or his BP worsens
    Brugada syndrome
    • Right bundle-branch block and ST elevation in the right precordial leads associated with ventricular fibrillation and sudden death
    • The underlying cause of BrS is a genetic defect in the SCN5A gene, which encodes the sodium channel controlling the depolarisation phase of the cardiac action potential.
    • There are usually no structural abnormalities in Brugada syndrome (BrS) patients and the disease may be defined as a pure electrical abnormality of myocardial cells.
    • BrS manifests with syncope and cardiac arrest typically occurring in the third and fourth decade of life, and usually at rest or during sleep.
    • Ajmaline test,,,Ajmaline is a class Ia antiarrhythmic agent. It is often used to bring out typical findings of ST elevations in patients suspected of having Brugada syndrome. Intravenous drug testing and electrophysiological testing for diagnostic confirmation
    • An implantable defibrillator is the treatment of choice in these patients,,,it may remarkably improve quality of life. Studies suggest that the majority of BrS patients are likely to remain asymptomatic and are at relatively low risk of relapsing.
    • patients may also be considered for therapy with quinidine, particularly those who present with "VF storm", with multiple firings of their defibrillator in one day.
    Syncope cardiac
    • The gold standard for diagnosis of an arrhythmic cause of syncope is documentation of a rhythm disturbance at the time of symptom occurrence.
    • The choice of monitoring test should be related to the frequency of the symptoms.
    • patient with recurrent, infrequent events; therefore, an implantable loop recorder would be the most likely test to result in a useful finding (either positive or negative).
    • An implanted loop recorder records patient-activated events and automatically records bradycardic and tachycardic events; it is, therefore, significantly less prone to acquisition errors than an event monitor. Implantable loop recorder batteries now last approximately 2 years.
    • The implantable loop recorder has repeatedly been shown to be cost effective and highly likely to result in a useful finding compared with a 24-hour ambulatory monitor or an event monitor.
    • External event monitors are of two types:
     loop monitors, which are worn and record continuously but only save when the patient activates the monitor, and
     hand-held event monitors, which must be held to the chest to record.
    o Loop monitors are useful for syncope because patient activation saves data from a short period of time (programmable and varying by company) before the monitor is activated by the patient.
    o Hand-held event monitors are not useful for syncope, since the patient cannot activate the monitor when consciousness is lost.
    Syncopy and ventricular arrhythmia
    • In the setting of a high enough clinical suspicion for syncope caused by ventricular arrhythmia, it is not necessary to formally document the arrhythmia with an event monitor before proceeding with ICD implantation, given the extremely high risk for sudden death in this setting.
    • In heart failure If the ejection fraction remained low after optimal medical therapy, the patient would also qualify for ICD implantation for a primary prophylaxis indication.
    Kawasaki disease
    • The condition is frequently self-limiting
    • but it is important to recognise, as it causes coronary arterial inflammation resulting in aneurysm formation (25% of cases) which may present much later in life.
    • Coronary disease can be prevented with treatment which includes non-steroidal anti-inflammatory drugs (NSAIDs) and gamma globulin infusion.
    Ischemic HD
    Patients with peripheral arterial disease have an increased risk of adverse cardiovascular event and frequently have coexistent coronary and cerebrovascular atherosclerosis; therefore it is considered a coronary artery disease equivalent. For this reason an appropriate statin should be commenced. Currently the recommended target is LDL less than 2.0 mmol/l,
    • Unstable angina Six-hour troponin T test may still miss some cases of unstable angina with troponin rise, as such 12-hour testing is recommended. Unless the electrocardiogram (ECG) changed significantly, IV heparin or IIB IIIA receptor antagonist therapy would not be indicated.
    • Recent studies have demonstrated that troponin T assay at the 12 hour stage is the most effective for cardiovascular risk stratification. If troponin T is normal (<0.03) at 12 hours it indicates very low forward cardiovascular risk. Mild elevation in the presence of ECG changes is supportive of a diagnosis of unstable angina and elevation of troponin T above a level of 0.1 indicates a confirmed myocardial infarction.
    • A normal echocardiogram between episodes of chest pain does not rule out unstable angina because wall motion returns to normal between ischemic episodes. However, if patient had no wall motion abnormalities during chest pain, an acute coronary syndrome is highly unlikely
    • β-Blockers are first-line therapy for unstable angina and NSTEMI unless contraindications are present.
    • With ongoing angina, a calcium channel blocker can be added to a β-blocker. However, there is no benefit in substituting a calcium channel blocker for a β-blocker in the absence of significant side effects.
    • Recent studies have suggested the possibility that angiotensin-converting enzyme inhibitors may be effective in reducing exercise-induced ischemia.
    • Recent randomized trials have shown that full-dose low-molecular-weight heparin is more effective than full-dose unfractionated heparin without an increase in bleeding events.
    • However, low-molecular-weight heparin is renally excreted, and if estimated glomerular filtration rate is below 30 mL/min/1.73 m2, the level of anti–factor Xa activity is increased, resulting in increased bleeding events. Full-dose unfractionated heparin is, therefore, preferable to full-dose low-molecular-weight heparin in patients with renal insufficiency.
    • Acute AMI,,,,,Primary angioplasty where available is the treatment of choice in this case. A number of studies have demonstrated its superiority over thrombolysis.
    • If the chest pain was associated with ST depression, then a IIb IIIa antagonist would be the correct answer.
    • If angioplasty is not available, then tenecteplase would be the best choice for thrombolysis.
    • Tissue plasminogen activator (TPA) has been shown to achieve better vessel patency than streptokinase in anterior myocardial infarction.
    Stable Angina
    • Elevated serum high-sensitivity CRP levels are an independent cardiovascular risk factor for myocardial infarction, stroke, and cardiovascular death, and are associated with development of metabolic syndrome and diabetes mellitus
    • In elderly patients Coronary angiography is usually reserved for patients who remain symptomatic in spite of medical therapy "add b blocker" as it carries significant risks in this age group
    • The β-blocker dose should be titrated to achieve a resting heart rate of approximately 55 to 60/min
    • Ranolazine Ranolazine is indicated for the treatment of Chronic angina. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current,,, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia in rats Unlike other antianginal medications such as nitrates and beta blockers, ranolazine does not significantly alter either the heart rate or blood pressure. For this reason, it is of particular use in individuals with angina that is refractory to maximal tolerated doses of other anti-anginal medications.
    • Ranolazine is known to increase the QT interval and is contraindicated in patients with preexisting QT-interval prolongation, liver disease, and in combination with drugs that prolong the QT interval or are inhibitors of CYP3A4, such as diltiazem and verapamil.
    • Ranolazine also prolongs the half-life of digoxin and simvastatin, and these drugs may require dose reduction.
    • Coronary angiography would not be indicated until the patient is receiving maximal medical therapy.
    • Coronary revascularization is beneficial in patients with chronic stable angina and the following conditions:
    o angina pectoris refractory to medical therapy;
    o a large area of ischemic myocardium and
    o high-risk criteria on stress testing;
     high-risk coronary anatomy, including left main coronary artery stenosis or three-vessel disease; and
     significant coronary artery disease with reduced left ventricular systolic function.

    Medically refractory angina on maximal medical therapy and is not a candidate for either percutaneous or surgical revascularization
    • Enhanced External Counterpulsation is a non-surgical treatment for Angina & Coronary Artery Disease. It is an alternative to bypass surgery and angioplasty. It works by stimulating the opening or formation of small blood vessels (collaterals) to create natural bypasses around narrowed or blocked arteries,,,,EECP uses three sets of pneumatic cuffs wrapped around the lower extremities to The cuffs are timed to inflate and deflate based on the individual's electrocardiogram. The cuffs should ideally inflate at the beginning of diastole and deflate at the beginning of systole. During the inflation portion of the cycle, the calf cuffs inflate first, then the lower thigh cuffs and finally the upper thigh cuffs. Inflation is controlled by a pressure monitor, and the cuffs are inflated to about 300 mmHg. When timed correctly, this will decrease the afterload that the heart has to pump against, and increase the preload that fills the heart, increasing the cardiac output.[4] In this way, ECP is similar to the intra-aortic balloon pump Contraindications to EECP include severe aortic regurgitation and severe peripheral vascular disease.
    • Spinal cord stimulation involves placement of an electrocatheter within the epidural space that is connected to a pulse generator and stimulates the spinal cord region receiving the cardiac nerve fibers. In a placebo-controlled trial, spinal cord stimulation was shown to reduce angina and improve functional status.
    Investigation for chest pain with history of IHD
    • Exercise stress test should be the first choice stressor for patients with good effort tolerance.
    • Myocardial perfusion imaging is indicated in the following situations:
    o high clinical suspicion with negative exercise test
    o low clinical suspicion with positive exercise test
    o borderline or uninterpretable exercise test
    o resting electrocardiogram (ECG) precludes stress ECG test eg left bundle branch block (LBBB).

    Ranolazine can be useful in patients with chronic stable angina on maximal medical therapy.

    Stent thrombosis causing myocardial infarction
    • Stent thrombosis usually occurs in the first two days after the procedure.
    • Combined antiplatelet therapy with aspirin and clopidogrel, reduces the risk of thrombosis.
    • Dual antiplatelet therapy with clopidogrel and aspirin is mandatory following placement of a coronary stent to reduce sudden thrombotic occlusion of the stent.
    • Clopidogrel is required for 1 month for bare metal stents and for 1 year for drug-eluting stents
    • This patient should be taken immediately to the Cardiac Catheterisation Lab with a view to performing
    o angioplasty or to
    o administer intracoronary thrombolytic therapy to open up the blocked stent.
    o Simultaneous use of abciximab (a glycoprotein IIb/IIIa inhibitor) has been shown to improve morbidity and mortality in acute coronary stent thrombosis
    • Emergency CABG might be considered if percutaneous intervention fails.
    • IV thrombolytic therapy is not the optimum therapy in this setting.

    Diabetes mellitus and ischemic heart disease
    • Coronary artery bypass grafting is indicated in patients with
     left main coronary artery disease,
     severe three-vessel disease with reduced left ventricular systolic function, and
     severe three-vessel disease with involvement of the proximal left anterior descending artery.
    o In this setting, surgery would not only relieve angina and improve quality of life, but it would also prolong life expectancy.
    o Patients achieve a significant clinical benefit when the left internal mamillary artery graft is used as the bypass for lesions within the left anterior descending artery system.
    • Enhanced external counterpulsation (EECP) is an acceptable treatment for patients with medically refractory angina who are not candidates for revascularization.
    Contrast-induced renal dysfunction
    • About 5% of patients undergoing cardiac catheterisation experience contrast-induced renal dysfunction.
    • Patients with diabetes and prior renal dysfunction are at increased risk.
    • Renal impairment increases the risk of accumulation of metformin and lactic acidosis.
    • Therefore, metformin should be stopped prior to coronary angiography and reinstated 48 h after the procedure if renal functions are found to be normal.
    Myocardial infarction
    • ST segment elevation in leads I and aVL is termed as high lateral wall MI and is usually the result of
    o occlusion of the first diagonal branch of the left anterior descending artery,
    o though occlusion of other arteries like branches of the left circumflex or a short left anterior descending artery may cause the same picture.
    • Low molecular weight heparin (LMWH) is the standard treatment in non-ST-segment elevation myocardial infarction (NSTEMI).
    • Despite the fact that LMWH is said to accumulate in renal failure, reduced dose LMWH have been shown to be effective in haemodialysis patients, as such it would still be an appropriate option here.
    • Management of cardiogenic shock
    o circulatory support in the form of vasopressors (IV dopamine) and
    o Intra-aortic balloon pump (IABP) and
    o reperfusion of the infarct-related artery.
    Diabetes and Myocardial infarction
    • Best Treat with IV insulin for 48hrs then consider restarting oral therapies
    • The DIGAMI(1) study suggested that using IV insulin for a short period, followed by S/c insulin therapy was associated with a survival benefit versus conventional glucose management.
    • This was not replicated in the later DIGAMI(2) study, where no benefit was seen from the DIGAMI regime versus conventional treatment of blood glucose.
    • The majority of clinicians now recommend only a short period of IV insulin therapy followed by a return to tablet treatment if the HbA1c was adequately controlled pre-myocardial infarction.
    • In patients with acute myocardial infarction with reduced left ventricular function (ejection fraction ≥40%) and clinical heart failure or diabetes mellitus, and who were on therapeutic doses of a β-blocker and an ACE inhibitor, the addition of eplerenone reduced total mortality and cardiovascular mortality.

    Post MI ventricular arrhythmia
    • If VT with unstable hemodynamic
    o give DC shock Then
    o IV lignocaine given as a bolus followed by infusion reduces myocardial automaticity and hence is the first choice for prophylaxis against a further episode of VT.
    o IV amiodarone would be the first choice alternative to lignocaine, especially where there is persistent hypotension.
    • Premature ventricular contractions (PVCs) and non-sustained ventricular tachycardia (NSVT) are common in the early post-myocardial infarction (MI) period.
    • NSVT is defined as three or more consecutive beats at a rate greater than 100 beats/min that last less than 30 s.
    • If these do not cause any haemodynamic compromise, treatment is not needed.
    • Hypokalemia increases the incidence of NSVT as well as VT and ventricular fibrillation (VF), hence it is prudent to check serum potassium (K+) levels early. During the GISSI-2 trial it was observed that a serum K+ level of less than 3.6 mmol/l was associated with a two-fold increased risk of VF. Therefore serum K+ should be maintained above 4 mmol/l by oral or intravenous (iv) supplementation in patients with acute MI.
    • Concomitant magnesium (Mg2+) deficiency is present in many patients with hypokalaemia and also makes correction of hypokalaemia difficult. Hence serum Mg2+ levels should also be checked and maintained above 1 mmol/l.
    • Antiarrhythmic therapy might be considered if NSVT causes haemodynamic compromise
    • Electrophysiological studies and implanting a cardiac defibrillator might be considered if NSVT occurs late (after 48 h) in the course of MI.
    • Results from the DINAMIT trial showed no benefit from cardioverter-defibrillator implantation early after myocardial infarction. For this reason, patients with reduced ejection fraction are not candidates for device placement within 40 days after acute myocardial infarction or immediately after percutaneous or surgical revascularization
    • Rescue angioplasty and emergency coronary artery bypass grafting (CABG) should be considered if there is evidence of failed thrombolysis or cardiogenic shock.
    •
    Right ventricular myocardial infarction
    • Inferior wall myocardial infarction (MI) is associated in one-third of cases with right ventricular myocardial infarction (RVMI).
    • RVMI leads to reduced right ventricle compliance and stroke volume, which in turn leads to reduced left ventricle filling and low cardiac output.
    • a pansystolic murmur is most likely to be a function of tricuspid regurgitation secondary to a hypokinetic dilated right ventricle.
    • Patients typically present with
    o hypotension,
    o jugular venous distension and
    o clear lung fields in the setting of an inferior or inferoposterior MI
    • These findings can mimic cardiac tamponade. An echocardiography will be useful in
    o excluding tamponade
    o demonstrating right ventricular dysfunction and dilatation.
    o It has an added advantage of assessing left ventricular ejection fraction.
    • Pulmonary embolism (PE) can also have similar physical findings that are jugular venous distension, hypotension and clear lung fields. However these findings occurring in a setting of inferior MI make PE less likely.
    • Treatment of right ventricular infarction includes early revascularization (PCI or thrombolytic therapy) to restore blood flow to the ischemic right ventricle
    • Even with successful revascularization, it can take up to 3 days for right ventricular function to return to normal.
    • Therapy for hypotension associated with RVMI involves
    o boluses of iv saline to improve right ventricular (RV) preload and cardiac output.
    o If up to 1.5 l of normal saline do not correct hypotension, invasive haemodynamic monitoring should be considered to guide further fluid therapy.
    o Similarly inotropic support may be considered after adequate fluid resuscitation has failed.
    o Nitroglycerin is contraindicated in patients with right ventricular myocardial infarction because of the potential for venodilation and hypotension.
    o iv Furosemide will reduce RV filling pressure and should be avoided.
    iv Heparin in combination with streptokinase does not confer any additional benefit and is not indicated.
    non ST segment elevation myocardial infarction
    • aspirin and Clopidogrel
    • Glycoprotein IIb/IIIa inhibitors should be administered in patients with NSTEMI who are at high risk of death and complications.
    • The high-risk features include:

    o age more than 70 years
    o prolonged rest pain
    o pulmonary oedema, hypotension or bradycardia
    o prior revascularisation
    o ST segment changes of greater than 1 mm or ventricular arrhythmias
    o elevated cardiac enzymes.
    • Other pharmacotherapy of NSTEMI includes
    o anticoagulation,
    o beta-blockers and
    o anti-anginals like nitroglycerine
    o angiotensin-converting enzyme inhibitors.
    Dressler syndrome
    • usually occurs 1 to 8 weeks after myocardial infarction.
    • Patients present with malaise, fever, pericardial pain, elevated erythrocyte count and sometimes may also have pleuritis and pneumonitis.
    • Results from release of cardiac antigens which then stimulate antibody production. The immune complexes are then deposited in the pericardium, pleura and lung.
    • Treatment involves Aspirin in large doses is effective.
    • Recurrences can occur, and in such cases colchicine is helpful.
    • Corticosteroids and non-steroidal anti-inflammatory agents are best avoided in the first 4 weeks after myocardial infarction as they delay myocardial healing.
    • There may be accompanying pleural and pericardial effusion and therefore echocardiography should be done. in the presence of significant effusion or if the effusion is increasing, heparin should be discontinued.
    • Anticoagulation can be continued if there is no pericardial effusion, as in such cases the risk of haemorrhagic pericarditis is low.


    Acute pulmonary oedema
    • The first step
    o high-flow oxygen,
    o furosemide 0.5–1 mg/kg intravenous (IV),
    o morphine 2–4 mg IV, and
    o sublingual nitroglycerine (GTN).
    • The second step is dictated by the systolic blood pressure (BP) after initial treatment:
    o If the BP is >100 mmHg, start IV nitroglycerine 10–20 µg/min;
    o BP of 70–100 mmHg, with no signs or symptoms of shock start IV dobutamine 2–20 µg/min;
    o BP is 70–100 mmHg with signs or symptoms of shock, start IV dopamine 5–15 µg/min;
    o BP is less than 70 mmHg with signs or symptoms of shock, start IV noradrenaline 0.5–30 µg/min.
    Flash pulmonary oedema
    • Rapidly developing pulmonary congestion
    • The most common cause of flash pulmonary oedema is myocardial ischaemia.
    Bilateral renal artery stenosis can also present with a similar clinical picture but is less common cause, as is acute aortic regurgitation.

    Tocolysis-associated pulmonary oedema
    • Tocolytics are medications administered for the suppression of premature contractions.
    • Acute pulmonary oedema can occur with administration of β2 agonists for tocolysis in up to 5–15% of cases.
    • It usually occurs after 24 h of administration of these agents.
    • The chest X-ray reveals pulmonary infiltrates and normal heart size.
    • Concomitant use of corticosteroids that are often administered for lung maturation have also been implicated as risk factor for development of tocolysis-associated pulmonary oedema.
    Treatment involves stopping the tocolytics, oxygen and careful volume control.


    Ventricular free wall rupture
    • Autopsy studies reveal that ventricular free wall rupture occurs about 10 times more frequently than postinfarction ventricular septal rupture, occurring in about 11% of patients following acute myocardial infarction.
    • Ventricular rupture and cardiogenic shock are now the leading causes of death following acute myocardial infarction, and together account for over two-thirds of early deaths in patients suffering their first acute infarction.

    Coronary stents re-stenosis
    • Studies have shown that in patients with type-2 diabetes, coronary stents are liable to re-stenosis at a rate of 40–50% by the end of a 6-month follow-up period.
    • Drug eluting stents have been shown to reduce the relative risk of re-stenosis by around 80%, but only where dual anti-platelet therapy with clopidogrel and aspirin is continued for at least 1 year.
    • Whilst there is evidence that both rosiglitazone and pioglitazone both reduce in-stent re-stenosis, rosiglitazone is not recommended in patients who have a history of previous myocardial infarction
    Risk factors for torsade de pointes include:
    • bradycardia,
    • hypokalaemia,
    • congestive heart failure,
    • digitalis therapy,
    • subclinical long-QT syndrome,
    • baseline QT prolongation,
    • severe hypomagnesaemia,
    • severe alkalosis and
    • recent conversion from atrial fibrillation.
    • Female sex is a powerful predictor of the risk of torsade de pointes in patients with congenital and acquired long-QT syndromes. How or whether variability in the expression of genes that determine normal cardiac electrophysiology explain the sex-dependent risk of torsade de pointes is not yet clear.

    Ventricular tachycardia (VT)
    • If secondary to digoxin toxicity and unstable haemodynamically. In the setting of digoxin toxicity DC cardioversion is not used unless all other measures have been exhausted because it is unusually unsuccessful. The most useful drugs in this setting are lidocaine and phenytoin. Amiodarone and procainamide may increase digoxin levels and should be avoided.

    Prolonged QT Interval
    • Six mutations (LQT1–6) have been identified in association with the Romano–Ward syndrome.
    • LQT1 and LQT2 mutations make up around 87% of cases of Romano–Ward syndrome and are associated with cardiac potassium-channel gene mutations.
    • JLN mutations (Jervell–Lange-Nielsen syndrome) tend to be associated with deafness.
    • Although sudden death usually occurs in symptomatic patients, it happens with the first episode of syncope in about 30% of the patients.
    • LQT4 is associated with paroxysmal atrial fibrillation.
    • Studies have shown an improved response to pharmacologic treatment with a lowered rate of sudden cardiac death in LQT1 and LQT2 compared with LQT3.
    • Triggering events are somewhat different by genotype.
    • Patients with LQT1 usually have cardiac events preceded by
    o exercise or swimming.
    o Sudden exposure of the patient's face to cold water is thought to elicit a vagotonic reflex.
    • Patients with LQT2 may have arrhythmic events after
    o an emotional event,
    o exercise, or
    o exposure to auditory stimuli (eg, door bells, telephone ring).
    • Patients with LQT3 usually have events during night sleep.
    • Diagnosis is based upon the QTc (corrected QT interval), although this may be within the normal range at rest; hence, Holter monitoring is recommended.
    • Genetic testing for known mutations in DNA samples from patients is becoming accessible in specialized centers.
    • Identification of an LQTS genetic mutation confirms the diagnosis. However, a negative result on genetic testing is of limited diagnostic value because only approximately 50% of patients with LQTS have known mutations. The remaining half of patients with LQTS may have mutations of yet unknown genes. Therefore, genetic testing has high specificity but a low sensitivity.
    • Beta-blockade is seen as the treatment of choice for most cases of long QT syndrome, which is thought to work through reducing adrenergic demand. Beta-blockers decrease sympathetic activation from the left stellate ganglion. Beta-blockers also decrease the maximal heart rate achieved during exertion and thereby prevent exercise-related arrhythmic events that occur in long QT syndrome.
    • Implantable defibrillators are also used in the management of these patients.
    • The activity of the left stellate ganglion is greater compared to the right stellate ganglion in normal individuals. Animal and human studies have shown that right stellectomy or primary increase in the output of the left stellate ganglion increases the QT interval.
    • Patients who experience ventricular arrhythmias or aborted sudden cardiac death despite beta-blocker therapy should have an implantable cardioverter defibrillator (ICD) in addition to beta-blockers.
    • Left stellate cardiac ganglionectomy is an invasive procedure and results in Horner’s syndrome. It is performed in patients who have symptoms despite beta-blockers and have frequent shocks with ICD.
    Dual chamber pacing might be beneficial in subset of patients with long QT syndrome type 3.
    • Management of drug-induced long QT syndrome is to
    o stop the precipitating drug,
    o correction of any electrolyte disturbance like hypokalaemia or hypomagnesaemia
    o treatment of associated ventricular arrhythmia.
    o First-line pharmacological therapy for drug-induced long QT syndrome is intravenous magnesium sulphate 2 g administered as bolus over 1–2 min, followed by another bolus in 15 min if required, or continuous infusion at a rate of 5–20 mg/min.
    •

    Prosthetic valve thrombosis (PVT)
    • May resulting in shock.
    • This complication occurs in 0.03 to 5.5% annually with equal frequency in bioprosthesis and mechanical valves.
    • It is more common in mitral prosthesis and with subtherapeutic anticoagulation.
    • The best diagnostic modality is transoesophageal echocardiography; however transthoracic echocardiography is the initial choice in sick patients, and if adequate visualisation is not obtained TEE can be done.
    • Thrombolytic therapy for patients
    o pulmonary oedema or
    o hypotension.
    o right-sided PVT should be treated with thrombolytic agents
    • surgery In
    o stable patients,
    o is a better option for left-sided PVT, while
    Serial echocardiography should be performed, and if the response is inadequate repeat thrombolytic therapy can be given.

    Complications of prosthetic valves include
    • structural valve deterioration, symptoms of heart failure with significant valve regurgitation.
    • valve thrombosis,
    • embolism,
    • bleeding,
    • pannus formation, is a slowly growing fibrous overgrowth fixed on the prosthesis, causing valve dysfunction
    • endocarditis.
    • prosthesis mismatch may occur when the inserted valve prosthesis is too small relative to patient size, recreating the outflow obstruction present preoperatively. The main hemodynamic consequence is persistence of significant transvalvular gradients through what is otherwise a normally functioning prosthesis.
    • Mild hemolytic anemia is common in patients with prosthetic heart valves, but can be more severe in up to 10% to 20% of patients.
    o Hemolytic anemia is more common in those with paravalvular regurgitation and with mechanical valves.
    o Clinical features include fatigue, anemia, new murmur, and, in more severe cases, jaundice and heart failure.
    o Most cases of hemolytic anemia are subclinical, identified only by laboratory data.
    o Symptomatic hemolytic anemia can usually be treated with oral iron and folate replacement, although more severe cases may warrant blood transfusion or recombinant human erythropoietin

    Anticoagulation for the pregnant patient with a mechanical valve prosthesis
    • when the dose of warfarin is less than 5 mg daily, the risk of embryopathy decreases to below 10%.So Continue warfarin, adjusted to INR


    Aortic stenosis
    • severe aortic stenosis
    o An absent aortic component of S2,
    o a long and late-peaking systolic murmur,
    o a sustained apical impulse
    • An overestimation of the severity of aortic stenosis can occur due to large volumes of blood passing over the valve at high velocities, which occurs in aortic regurgitation.
    • Aortic valve replacement is not performed in asymptomatic patients because of the increased surgical risk
    • Patient with severe left ventricular (LV) dysfunction, and calculated valve area in such patients can be falsely low because low cardiac output reduces the valve opening forces.
    • It is important to distinguish patients with true severe aortic stenosis (AS) with secondary LV dysfunction from those who have a falsely low calculated aortic valve area because of low cardiac output.
    • An important method of distinguishing between the two conditions is to assess the haemodynamics after increasing the cardiac output by dobutamine infusion during echocardiography or cardiac catheterisation.
    • Patients with truly severe AS manifest an increase in transaortic pressure gradient while the valve surface area remains the same during dobutamine infusion; while those with falsely low calculated valve area manifest an increase in calculated valve surface area.
    • Dobutamine echocardiography is also important to assess LV contractile reserve. Patients who have 20% or more increase in stroke volume after dobutamine infusion have a much better prognosis after surgery compared to those who do not have LV contractile reserve.

    Aortic stenosis with acutely ill elderly patient with heart failure
    • The ultimate treatment is valve replacement but in a patient who is acutely unwell, a valvuloplasty is used as a bridging procedure.
    • An aortic balloon pump would improve the cardiac failure and also increase coronary perfusion, and is necessary in such a high-risk procedure.
    • Noradrenaline has no place here as it can worsen the left ventricular failure as raising the afterload may cause the ventricle to fail further. Milrinone, a phosphodiesterase III inhibitor, appears to be useful in moderate ventricular dysfunction with small doses of adrenaline. This increases the cardiac output as well as raising the mean arterial pressure.

    Microcytic anaemia and severe calcific aortic stenosis
    • This is Heyde’s syndrome
    • The treatment is to replace the valve after blood transfusion " No further gastro-endoscopies are needed", as the mechanism is thought to be due to destruction of von Willebrand’s factor as the platelets traverse the stenosed valve resulting in bleeding per rectum.
    • several gastric endoscopies and colonoscopies in search of an underlying cause of his anaemia may be done with –ve results
    • The investigation of choice after valve replacement is mesenteric angiography as the bleeding vessels are poorly visualised on colonoscopy. This would look for the presence of angiodysplasia, which may be associated with aortic stenosis. Resection of the diseased bowel has also been described as a treatment


    Mitral stenosis
    • Clinical markers consistent with severe mitral stenosis are
    • transmitral pressure gradients greater than 10 mm Hg,
    • enlargement of the left atrium,
    • mitral valve area less than 1.5 cm2, and
    • pulmonary pressures greater than 50 mm Hg.
    Clinical outcome in
    • asymptomatic or minimally symptomatic patients with mitral stenosis is excellent (>80% survival at 10 years),
    • but once patients are symptomatic, 10-year survival is less than 15%.
    • Morbidity associated with untreated mitral stenosis includes
    o pulmonary hypertension,
    o right-sided heart failure,
    o systemic embolism from atrial fibrillation, and
    o valve infection.
    Management
    • In symptomatic patients, percutaneous valvuloplasty is the preferred
    • less invasive than surgical intervention
    • avoids the need for lifelong anticoagulation.
    o Major complications of percutaneous valvuloplasty include
    • severe mitral regurgitation (1%-8%)
    • systemic embolization (1%-3%)
    • tamponade (1%-2%).
    • Procedural mortality rate is 1%.
    o Valve characteristics that favor successful valvuloplasty include
    • pliable mitral valve leaflets,
    • minimal commissural fusion, and
    • minimal valvular/subvalvular calcification,
    o These are contraindications:
    • severely calcified or
    • rigid valve leaflets,
    • concomitant coronary artery or other valve disease requiring surgery.
    • concomitant mitral regurgitation.
    • atrial thrombus
    • In patients under consideration for valvuloplasty, transesophageal echocardiography is necessary to definitively exclude a left atrial thrombus because of the risk of thrombus dislodgement and embolization during the procedure.
    • If thrombus present These patients should undergo mitral valve replacement.

    Mitral stenosis with paroxysmal AF
    • A beta-blocker can be used as first-line treatment, as it might prevent atrial tachyarrhythmias. It will also slow down the heart rate in sinus rhythm, thus increasing diastolic time and augmenting cardiac output.
    • Digoxin is not particularly helpful in paroxysmal AF, and
    • amiodarone should be reserved for resistant cases.

    Mitral regurgitation
    • Clinical markers that should prompt surgical intervention include
    o left ventricular enlargement or dysfunction (end-systolic dimension >40 mm and ejection fraction <60%),
    o new-onset atrial fibrillation,
    o pulmonary arterial systolic pressure >50 mm Hg, or
    o an exercise-associated increase in pulmonary pressures (increase of approximately 25 mm Hg over baseline).
    • Otherwise, asymptomatic patients with severe, chronic mitral regurgitation but normal left ventricular size and function can be reevaluated with periodic 6- to 12-month monitoring.


    Decompensated rheumatic mitral valve disease in pregnancy
    • optimization of medical management is preferred over urgent percutaneous mitral balloon valvuloplasty.
    • A transthoracic echocardiogram aids in evaluating the severity of mitral stenosis, pulmonary pressures, involvement of other cardiac valves, and the presence of concurrent mitral regurgitation.
    • If the patient can be treated medically and the pregnancy carried to term, valvuloplasty can be delayed until after delivery to reduce radiation exposure to the fetus and provide an opportunity to reassess the patient.
    • With the decrease in volume load, a previously symptomatic pregnant patient may improve following delivery, delaying or eliminating the need for valvuloplasty.
    • If despite aggressive medical therapy, the pregnant patient remains severely symptomatic, however, percutaneous balloon valvuloplasty may be performed (preferred gestational age >8 weeks) if significant mitral regurgitation is absent and a left atrial thrombus is excluded by transesophageal echocardiography.
    Peripartum cardiomyopathy
    • Peripartum cardiomyopathy is defined as heart failure with a left ventricular ejection fraction less than 45% that is diagnosed between 3 months before and 6 months after delivery in the absence of an identifiable cause.
    • Risk factors for peripartum cardiomyopathy include
     age (>30 years at the time of the pregnancy),
     race (black, African, Haitian), and the
     presence of gestational hypertension.
    • With a maternal mortality rate of approximately 10%,
    • Improvement in left ventricular function occurs in about 50% of women with peripartum cardiomyopathy within 6 months after delivery.
    • Treatment is the same as for the non-pregnant patient with cardiac failure, although angiotensin-converting enzyme inhibitors should be avoided.
    • The mainstay of medical treatment is digoxin and loop diuretics.
    • Nitrates are generally not recommended during pregnancy. If indicated nitrates and inotropic support with dobutamine should be used.
    • Beta-blockers should be added once the patient’s volume status is optimised.
    • Patients with PPCM are at risk of thromboembolism due to both hypercoagulable state of pregnancy and stasis of blood in the left ventricle. Therefore, anticoagulation with heparin or warfarin is recommended "when left ventricular ejection fraction is less than 35%". Heparin is preferable in late pregnancy because it has short half-life and can be discontinued prior to delivery.
    • Intravenous immune globulin and pentoxifylline have been shown to improve outcomes in some studies.
    Dilated cardiomyopathy
    • The prevalence of is approximately 1%, and incidence increases with age and approaches 10% at the age of 80 years.
    • Annual mortality associated with cardiomyopathy and moderate heart failure is 20%
    • Signs at clinical presentation include increased jugular venous pressure (JVP), small pulse pressure, hepatomegaly and peripheral oedema, and functional mitral regurgitation is often present.
    • Predisposing factors include
    o alcoholism,
    o viral myocarditis,
    o cocaine abuse, and toxins such as cobalt, lead, phosphorus and carbon monoxide.
    • Heart failure should be managed with diuretic therapy, sodium restriction and ACE inhibition.
    • Crucial to the management of alcoholic cardiomyopathy is cessation of alcohol use.
    • Patients who succeed in giving up ethanol often gain rapid improvement in their symptoms.
    Hypertrophic obstructive cardiomyopathy
    • The disease exists in two major forms:
    o a familial one that presents in young patients and has been mapped to chromosome 14q, and
    o a sporadic form usually found in the elderly.
    • Symptoms of cardiac failure respond to medical therapy with
    o b-blockade use metoprolol ,,,,BUT Carvedilol has vasodilator properties that could further lower blood pressure as well as potentially exacerbate outflow gradient.
    o but where the outflow gradient is greater than 50 mmHg, surgical myomectomy is usually recommended.
    o Unfortunately surgery does not reduce the risk of arrhythmia.
    o Surgical septal myectomy should be considered in patients with outflow obstruction who are NYHA functional class III or IV and whose symptoms are refractory to medical therapy.
    • Patients prone to ventricular arrhythmias may be considered for implantable defibrillator.
    Common ECG findings in patients with HOCM include
    1. LV hypertrophy,
    2. atrial enlargement,
    3. ST-T segment abnormalities,
    4. right or left axis deviation,
    5. PR prolongation,
    6. sinus bradycardia with ectopic atrial rhythm and bundle branch block.
    7. Ventricular fibrillation is responsible for the sudden death in 80% of these patients.
    8. HOCM can also be associated with Wolff–Parkinson–White syndrome

    Cardiac amyloidosis
    • most commonly presents as restrictive cardiomyopathy.
    • The clinical findings are those of right heart failure ie jugular venous distension and peripheral oedema,
    • whereas orthopnoea and paroxysmal nocturnal dyspnoea are typically absent.
    • In more advanced stages systolic dysfunction also occurs.
    • Postural hypotension can occur as a result of
    o poor ventricular filling or
    o associated autonomic neuropathy.
    • Combination of low-voltage electrocardiogram (ECG) and thickened ventricular walls is one of the characteristic features of cardiac amyloidosis.
    • The most distinctive feature of cardiac amyloidosis is a sparkling, granular appearance of the myocardium, but this is a relatively insensitive feature occurring only in about 25% of cases.
    • Other echocardiographic abnormalities include dilatation of atria, thickened interatrial septum, diastolic dysfunction and small-volume ventricles.
    • Cardiac amyloidosis usually occurs in setting of light chain amyloidosis (AL) and hereditary amyloidosis, and rarely in secondary amyloidosis.

    Hypertension
    • beta-blocker diuretic combination is not recommended due to an association with incident diabetes in BP lowering meta-analyses.
    • Every patiente with type 2 diabetes above 40 years of age should be treated with a statin unless contraindicated.
    • Lowering diastolic blood pressure should be gradual and cautious in patients with coronary artery disease or diabetes mellitus and in those who are older than 60 years, to avoid the possibility of inducing myocardial ischemia. Although lower systolic blood pressure measurements are associated with better outcomes in ischemic heart disease, there is inconsistent evidence that excessive diastolic blood pressure lowering may worsen cardiac outcomes.
    • accelerated hypertension
    o should be admitted to hospital
    o Initial treatment can be with ORAL nifedipine or atenolol, escalating to intravenous therapy with nitrates if there is no effect.
    o Sublingual nifedipine should be avoided as it might lead to a sudden drop in blood pressure, which could interfere with the autoregulatory mechanism of cerebral perfusion leading to an ischaemic stroke.
    • Hypertensive encephalopathy with a deteriorating level of consciousness conscious level.
    o condition is too advanced for oral therapy and requires intravenous (iv) blood pressure lowering therapy with sodium nitroprusside.
    o The aim of treatment is to lower blood pressure to around 110–115 mmHg diastolic within 2–4 h.
    o Nitroprusside therapy is usually accompanied by iv furosemide.



    How should I manage a woman with chronic hypertension?
    Advise the woman that:
    • She should restrict her dietary intake of salt (sodium)..
    • Bed rest is not recommended.
    • For uncomplicated hypertension, keep the blood pressure less than 150/100 mmHg (but diastolic pressure no less than 80 mmHg).
    • If there is evidence of target-organ damage (for example kidney disease), keep the blood pressure less than 140/90 mmHg.
    • Warn about symptoms of pre-eclampsia and that she should seek immediate advice if she develops any symptoms after 20 weeks' gestation (including during the postpartum period).
    • Prescribe aspirin 75 mg daily from 12 weeks' gestation. Explain that this is believed to help prevent the development of pre-eclampsia.



    • Acute mountain sickness,
    o one manifestation of which is acute pulmonary oedema.
    o oxygen would be initiated first, particularly in view of persistent hypoxia
    o Nifedipine reduces pulmonary hypertension and is the treatment of choice for pulmonary oedema in cases where high-flow oxygen is not available.
    o Acetazolamide may be of some value in prophylaxis in preventing acute mountain sickness, but the best prevention is slow acclimatisation.
    o Patients may also present with high altitude cerebral oedema, the treatment for which is dexamethasone. Where available, portable pressure bags are a useful adjunct to therapy.



    Congestive cardiac failure
    •
    • BNP may be elevated with
    • heart failure,
    • acute myocardial infarction
    • pulmonary embolism.
    Obesity is associated with lower BNP levels
    BNP levels are higher in the settings of
    • renal failure,
    • older age, and
    • female sex.
    • A calcium antagonist such as amlodipine precipitates peripheral oedema and fluid retention and should be withdrawn.
    • Digoxin is a last resort in patients with no evidence of atrial fibrillation.
    • A beta-blocker such as bisoprolol offers great prognostic benefit but should be initiated during a stable stage of the condition.
    o Beta-blocker should be initiated in small doses and in stable patients who have little or no evidence of fluid overload. Once started, patients should be monitored for worsening of symptoms or fluid retention.
    o Patients should be educated about possible worsening of symptoms and to weigh themselves daily.
    o If worsening of symptoms or fluid retention occurs, it should be managed by increasing the dose of diuretics
    o Stopping the beta-blocker is only required if there is
    • heart block,
    • hypotension or
    • severe pulmonary oedema.
    o It is better to try and continue the beta-blocker if possible.
    • For patients intolerant of ACE inhibitors due to hyperkalemia or renal insufficiency, the combination of hydralazine and a nitrate is a suitable alternative, with hemodynamic effects of vasodilation and afterload reduction. Treatment with this combination is also associated with a reduction in mortality
    • The addition of hydralazine and isosorbide dinitrate to standard medical therapy is indicated for treatment of black patients with systolic heart failure and New York Heart Association functional class III or IV symptoms.
    • Thiazide diuretics should be used very cautiously if there is no satisfactory diuresis on furosemide alone
    • Spironolactone combines a good diuretic effect with prognostic benefit. In this case it will also help raise the patient’s potassium.
    • Alpha-blockers and nitrates are alternatives for patients who do not tolerate first-line agents.
    • Clinical studies have not demonstrated that the combination of captopril and valsartan improves survival, and the combination is associated with an increased incidence of side effects.
    • Endomyocardial biopsy is recommended in patients with
    o new-onset heart failure (<2 weeks) with hemodynamic compromise and
    o in those with new-onset heart failure of 2 weeks’ to 3 months’ duration associated with a
    • dilated left ventricle and
    • new ventricular arrhythmias,
    • Mobitz type II second- or third-degree atrioventricular heart block, or
    • failure to respond to usual care within 1 to 2 weeks.
    Heart failure on maximal medical therapy.
    Other options
    • biventricular pacing " cardiac resynchronization"
    o ejection is less than 35%,
    o there is refractory heart failure
    o QRS complex duration >120 ms.
    • biventricular implantable cardiac defibrillator (ICD)
    o if there is evidence of previous ischaemic heart disease and ventricular arrhythmias.
    o Current guidelines recommend implantable cardioverter-defibrillator (ICD) placement in patients with ischemic or nonischemic cardiomyopathy and an ejection fraction of less than or equal to 35%. ICD placement is, therefore, indicated in this setting (primary prevention), regardless of symptoms or functional status
    • Biventricular pacemaker-defibrillator placement
    o Approximately 70% of patients who undergo biventricular device placement obtain a symptomatic benefit, thought to result from mechanical “resynchronization†of the timing of right and left ventricular contraction.
    o These devices have been shown to improve
    • ejection fraction,
    • quality of life, and
    • functional status,
    • decrease heart failure hospitalizations and mortality.
    • A ventricular assist device is an alternative to transplantation. The criteria includes
    o history of cardiogenic shock,
    o pulmonary capillary wedge pressure >20 mmHg, and
    o either a cardiac index <2.0 l/min/m2 or a systolic blood pressure <80 mmHg despite maximal inotropic support.

    The indications for biventricular pacemaker-defibrillator placement include NYHA class III or IV heart failure, an ejection fraction less than or equal to 35%, and a QRS width greater than 120 msec. Approximately 70% of patients who undergo biventricular device placement obtain a symptomatic benefit, thought to result from mechanical “resynchronization†of the timing of right and left ventricular contraction. These devices have been shown to improve ejection fraction, quality of life, and functional status, as well as to decrease heart failure hospitalizations and mortality.


    Hyponatraemia in heart failure
    • is associated with poor outcomes.
    • Patients with congestive heart failure (CHF) have decreased cardiac output and effective blood circulating volume. This results in activation of the renin–angiotensin system and release of antidiuretic hormone (ADH) and subsequent failure of excretion of ingested water.
    • Water restriction is the first-line and mainstay of therapy in hyponatraemic patients with CHF.
    • Stopping furosemide will not be possible for a patient who has decompensated heart failure.
    • Similarly, administration of hypertonic saline is only indicated if there is neurological manifestation of hyponatremia. Moreover hypertonic or isotonic saline administration will be poorly tolerated in a volume-overloaded patient.
    • Lithium can inhibit the action of ADH, but has slow onset of action and numerous central nervous system and cardiotoxic effect
    Endocarditis

    Endocarditis: initial ‘blind’ therapy
    1. Flucloxacillin (or benzylpenicillin if symptoms less severe) + gentamicin
    2. cardiac prostheses present, or if penicillin- allergic, or if meticillin-resistant Staphylococcus aureus suspected "vancomycin + rifampicin"
    Endocarditis caused by staphylococci
    1. Flucloxacillin 4 weeks
    2. if penicillin allergic or if meticillin-resistant Staphylococcus aureus "vancomycin + rifampicin" 6 weeks
    3. prostheses vancomycin + rifampicin+Gentamicin

    Endocarditis caused by streptococci

    1. Benzylpenicillin "4wk" + gentamicin"2wk" (if no intracardiac abscess or infected emboli
    2. Benzylpenicillin "6wk" + gentamicin"2wk" prostheses
    3. if penicillin- allergic or highly penicillin-resistant vancomycin + gentamicin

    Endocarditis caused by enterococci (e.g. Enterococcus faecalis)
    1. Amoxicillin + gentamicin 4wk
    2. Amoxicillin + gentamicin 6 wk prosthetic
    3. if penicillin-allergic or penicillin-resistant vancomycin + gentamicin
    4. if gentamicin-resistant, substitute gentamicin with streptomycin

    Endocarditis caused by haemophilus, actinobacillus,
    cardiobacterium, eikenella, and kingella species
    (‘HACEK’ organisms)
    1. Amoxicillin+ low-dose gentamicin
    2. if amoxicillin-resistant ceftriaxone + low-dose gentamicin


    Candida endocarditis
    • Risk factors
    o Intravenous drug abuse,
    o immunodeficiency states and
    o indwelling catheters
    • The aortic valve is the most common valve to be involved.
    • Optimum management involves
    o intravenous (iv) amphotericin for at least 6 weeks and
    o early surgery.
    o Despite this, recurrences can occur.
    Conditions in which surgery should be done for optimum management in the setting of infective endocarditis include
    o congestive heart failure
    o organisms that are difficult to eradicate by medical therapy as such
    • fungi,
    • brucella, coxiella,
    • pseudomonas aeruginosa,
    • vancomycin-resistant enterococci
    o vegetations greater than 1 cm in diameter (which pose an embolic risk),
    o recurrent embolisation
    o persistent bacteraemia despite appropriate antibiotic therapy
    o extension of infection to a extravalvular site "paravalvular extension"
    o early prosthetic valve endocarditis (within 2 months)
    o Patients with fever and a prosthetic valve should be treated presumptively for endocarditis unless a clear alternative source of infection is present. Surgery should not be delayed to complete an antibiotic course if surgical criteria are met
    o dehiscence or obstruction of a prosthetic valve.
    Bacteroides fragilis endocarditis
    • is a rare complication associated with colonic resection.
    • As passage of bacteria to the heart occurs via venous drainage, valve lesions tend to be right sided but may also occur as here on the left side of the heart. In this case the mitral valve lesions have lead to mitral regurgitation.
    • Management of choice is with metronidazole.
    • The incidence of post-op endocarditis is actually very low because of the use of peri-operative broad-spectrum antibiotics, normally the combination of a cephalosporin and metronidazole.


    Acute respiratory distress syndrome
    • may be secondary to a fat embolus in frctures
    • clinically there may be
    o coars
  15. Dr albarwari

    Dr albarwari Guest

    CARDIOLOGY

    Acute respiratory distress syndrome
    • may be secondary to a fat embolus in frctures
    • clinically there may be
    o coarse crackles on auscultation of his chest bilaterally.
    o jugular venous pressure is raised
    o There is no peripheral oedema.
    o ECG shows right axis deviation with prominent R waves on leads V1–V2.
    • Initial resuscitation should involve
    o high flow oxygen and
    o intravenous (iv) fluids to maintain high right ventricular filling pressures.
    o Steroid therapy is normally used a little later in ARDS, it can worsen pulmonary oedema.
    o Continuous positive airways pressure ventilation would help in the management of the pulmonary oedema.
    o It should be noted that diuretic treatment would be strongly contraindicated "even in pulmonary oedema". This is because the right ventricular output is dependent on elevated filling pressures. Reducing the preload is therefore not a good idea.

    Mitral stenosis
    MS with AF
    • Patients tolerate fast atrial fibrillation very poorly.
    • Treatment
    o oxygen
    o achieve rate control as quickly as possible. This is most quickly achieved with the use of a short-acting beta-blocker such as esmolol through a continuous infusion This might seem counter-intuitive in a hypotensive patient, but the hypotension is rate dependent as the ventricle has no time to fill.
    o Digoxin takes a few hours to act whether given orally or intravenously.
    o Amiodarone also takes a few hours to act
    o Flecainide is contraindicated in patients with structural cardiac abnormalities.
    o DC cardioversion should be considered if the patient does not respond quickly.


    Aortic regurgitation
    • All symptomatic patients with severe AR should have AVR.
    • Asymptomatic patients with severe AR should also undergo AVR if they have
    o depressed left ventricular (LV) function (ejection fraction (EF)<50%) or
    o if they have severe LV dilatation (end-diastolic dimension >75 mm and end-systolic dimension >55 mm).
    • Similarly patients with severe AR undergoing coronary artery bypass grafting or surgery on the aorta or any other valve should have AVR at the time of surgery.
    • Vasodilator therapy in the form of angiotensin-converting enzyme inhibitors or nifedipine should be given to patients who do not have indications for AVR.
    • Patients with AR require regular echocardiographic follow-up to assess the state of the left ventricle, as symptoms develop quite late in the course of the disease. so regular echocardiographic follow-up is required to pick up individuals with early features of left ventricular failure "dilated left ventricle, an ejection fraction of ≤50%" that would benefit from valve replacement.
    • Acute severe aortic regurgitation is a surgical emergency, necessitating valve replacement, particularly with symptoms of heart failure.

    Severe Aortic stenosis with noncardiac surgery
    • prophylactic valve replacement is not performed in asymptomatic patients. In patients with significant aortic stenosis but with good preoperative exercise tolerance, non cardiac surgical procedures are generally well tolerated
    • Rarely, valvuloplasty is considered in patients with severe, symptomatic aortic stenosis who require emergent noncardiac surgery and are not candidates for valve replacement.
    • Percutaneous aortic balloon valvuloplasty is generally not performed for calcific aortic stenosis because serious complications, including aortic regurgitation and embolic stroke, occur in more than 10% of procedures, and restenosis occurs within a year in most patients.
    • ACE inhibitor therapy is contraindicated in severe AS.

    Mitral valve prolapse
    • Patients under 75 with mitral valve prolapse (MVP) who are in atrial fibrillation or those who have echocardiographic evidence of left ventricular impairment should be referred for surgical assessment as early as possible.
    • A TOE can demonstrate whether the valve is amenable to repair or needs replacement. This is often performed intra-operatively.
    • Progressive mitral regurgitation is the most serious complication occurring in about 15% of patients over a 15-year period.
    • Acute hemiplegia, transient ischaemic attacks, cerebellar infarcts, amaurosis fugax and retinal arterioral occlusions all occur more frequently in MVP patients, suggesting that cerebral emboli are actually quite common in this condition


    Pulmonary valve stenosis
    • The diagnosis of pulmonary valve stenosis is confirmed by transthoracic echocardiography.
    • Echocardiography with Doppler evaluation determines the severity of pulmonary stenosis and the degree of right ventricular hypertrophy.
    • Intervention is recommended when
    o the gradient is greater than 50 mm Hg or
    o when right ventricular hypertrophy is present.
    • Systolic doming of the pulmonary valve noted on two-dimensional echocardiography suggests that the valve is likely amenable to percutaneous intervention.
    • The treatment of choice for pulmonary valve stenosis is pulmonary balloon valvuloplasty.

    Acute pericarditis.
    • ECG differential diagnosis of acute pericarditis is myocardial infarction and early repolarisation abnormality.
    • It can be differentiated from myocardial infarction by
    o concavity of ST segment elevation in pericarditis
    o localisation of ST segment elevation to infarction
    • However, these two features do not differentiate acute pericarditis and early repolarisation abnormality.
    • The two most helpful differentiating features are
    o PR segment depression, which is usually best seen in lead II and V6, and PR segment elevation in aVR.
    o An ST/T ratio greater 0.25 or a T wave amplitude of less than or equal to 3 mm also has high positive and negative predictive value in diagnosis of acute pericarditis
    • Between 15% and 30% of patients with apparently idiopathic acute pericarditis may have recurrent attacks and this is considered to be an autoimmune phenomenon.
    • Echocardiogram is of little value in the diagnosis of pericarditis. It can be used if a pericardial effusion or aortic dissection is suspected.
    • The mainstay of therapy for acute pericarditis is pain relief with NSAIDS like indomethacin "not paracetol"
    • Colchicine is useful both in acute episode and to prevent recurrence of pericarditis.
    • Prednisolone can be considered in patients who fail to respond to non-steroidal anti-inflammatory drug and colchicine therapy.
    • Pericardectomy is only indicated once thorough medical therapy has failed.
    • Pericardial biopsy in patients with recurrent pericarditis without effusion is unlikely to be revealing and is not needed

    Constrictive pericarditis
    • It is important to consider use of corticosteroids in conjunction with anti-tuberculous therapy early in these patients, as there is some evidence that steroids may reduce the risk of constrictive pericarditis.
    • Surgical pericardial biopsy is most likely the investigation to determine the underlying diagnosis

    Pericardial effusion, management
    • In the absence of cardiac tamponade,
    o pericardiocentesis may be indicated if clinical suspicion exists for bacterial, tubercular, or systemic inflammatory causes of pericarditis.
    • In patients with an isolated pericardial effusion
    o An idiopathic pericardial effusion lasting less than 3 months in a stable patient requires no specific therapy, but serial echocardiography based on clinical status, is advisable.
    o Pericardiocentesis is warranted if an effusion persists for longer than 3 months and may be curative in approximately 50% of patients with idiopathic effusions. In addition, pericardiocentesis prevents the development of cardiac tamponade.

    Myocarditis

    There is no specific treatment for idiopathic (also called lymphocytic) myocarditis other than supportive care and standard therapy for heart failure; thus, therapy with an angiotensin-converting enzyme (ACE) inhibitor such as captopril and a β-blocker such as carvedilol would be appropriate to start

    Dilated cardiomyopathy
    • If secondary to alcohol abuse, Abstinence from alcohol and angiotensin-converting enzyme (ACE) inhibitor therapy are paramount in arresting the progress of the condition.
    • Before a diagnosis of dilated cardiomyopathy can be made, any occult coronary artery disease should be excluded

    Restrictive cardiomyopathy
    • Digoxin is contraindicated in amyloid patients as patients are extremely sensitive to it. This is possibly due to digoxin binding in the amyloid fibrils.
    • Hemochromatosis is the only cause of restrictive cardiomyopathy that is potentially reversible by medication therapy that induces regression of symptoms.
    • Restrictive cardiomyopathy from iron overload may improve with removal of iron by chelation therapy in iron-overload states, such as lifelong transfusion-dependent anemias.
    • Iron chelation therapy is indicated only in patients who cannot tolerate phlebotomy therapy, such as those with significant anemia.
    • In hereditary forms of hemochromatosis, iron overload is appropriately treated by phlebotomy. Phlebotomy effectively removes excess iron and circumvents the need for chelation therapy. However, phlebotomy would not be appropriate for this patient with acquired hemochromatosis and sickle cell anemia.
    • Echocardiographic findings evidenced by
    o restrictive left ventricular filling without respiratory variation in peak filling velocity,
    o biatrial enlargement, and
    o preserved ventricular systolic function.
    • Endomyocardial biopsy is positive for iron deposition in this patient, but this biopsy finding is not invariably present because iron deposition is often predominantly in the epicardial layer. Thus, a negative endomyocardial biopsy would not exclude myocardial iron infiltration.

    Atrial myxoma
    • finger clubbing,
    • normocytic anaemia,
    • a positional murmur and
    • intracardiac calcification in the chest X-ray.
    • The history of fainting spells suggests transient left ventricular inflow obstruction.
    • The patient should undergo urgent echocardiography and be referred for surgery if the diagnosis of myxoma is confirmed, as complete removal is curative.

    Primary pulmonary hypertension
    • young women with worsening breathlessness.
    • The presence of exertional chest pain (right ventricular angina), Raynaud’s phenomenon in combination with the clinical and ECG features of right ventricular hypertrophy point towards PPH.
    • Chronic thromboembolic disease and respiratory disease should be excluded before the diagnosis can be made.
    • pregnancy
    o The patient should be advised against pregnancy.
    o Severe pulmonary hypertension in pregnancy has high mortality approaching 50%,
    o Patients who opt against termination of pregnancy should be closely followed up and managed with anticoagulation, oxygen and pulmonary vasodilator therapy like prostacyclin.
    o Bosentan is teratogenic and should not be used in pregnancy.
    o The patients should be advised for contraception in future, but oral contraceptive pills should not be used for possible increased risk of thrombo-embolism.
    • Treatment of PPH consists of
    o oxygen,
    o anticoagulation,
    o high-dose calcium channel blockers in patients responsive to acute vasodilator testing and
    o intravenous/nebulised prostacyclin to non-responders. Continuous infusion of prostacyclin has been shown in prospective studies to improve quality of life and symptoms related to PPH, exercise tolerance, haemodynamics and survival.
    o A combined lung–heart transplant is the last resort for those who fail to respond to any other treatment.
    o Anticoagulation, prostacyclin and transplant all confer a survival benefit.

    Aortic dissection
    • central chest pain radiating to the back
    • Ascending aortic dissection is often associated with
    o acute aortic regurgitation,
    o myocardial ischemia inferior MI (involvement of the right coronary artery)
    o cardiac tamponade or
    o hemopericardium, and
    o hemothorax or exsanguination.
    o Considerable (>20 mm Hg) variation in systolic blood pressure in the arms may be present.
    • Descending thoracic aortic aneurysm is more commonly associated with
    o splanchnic ischemia,
    o renal insufficiency,
    o lower extremity ischemia, or
    o focal neurologic deficit due to spinal cord ischemia.
    • The absence of a widened mediastinum on chest X-ray does not rule out dissection.
    • The diagnosis can be further suggested by the finding of aortic regurgitation and pericardial effusion, or even a dissection flap, in the echocardiogram. This can be done by the bedside while steps are taken to prepare the patient for theatre, and as such is much safer than a computerised tomography with contrast in the first instance.
    • Patients with type A aortic dissection should have emergency surgery because of the high risk of mortality and complication such as
    o aortic regurgitation,
    o myocardial infarction and
    o cardiac tamponade.
    • Most patients with type B dissection should be treated medically unless they have complications such as persistent leak, rupture or compromised blood flow to renal, mesenteric or limb circulation.
    o Beta-blockers are the mainstay of medical therapy, as they
    • reduce the rate of left ventricular ejection and shear on the aortic wall.
    • The aim is to reduce blood pressure to 100–120 mmHg and the pulse to near 60 mmHg.
    o Sodium nitroprusside can be added if blood pressure is not controlled with beta-blockers but should not be used alone as it may increase rate of left ventricular ejection. Hydralazine should be avoided for the same reason.



    Features that favour oesophageal rupture over aortic dissection include:
    • The history of onset while eating
    • Blood pressure equal in both arms
    • No diastolic murmur
    • Good peripheral pulses
    • Presence of a pleural effusion.

    Carcinoid syndrome
    • Markedly elevated HIAA concentrations are typically found and do not reflect a worse prognosis.
    • Mild derangement of AST/ALT is typically found and alkaline phosphatase is often elevated as a consequence of carcinoid infiltration and mild obstruction.
    • Liver function is usually quite normal despite often heavy hepatic infiltration.
    • Wheeze, again, is a typical feature as a consequence of the release of vasoactive compounds such as 5-HT and bradykinin.
    • Symptoms usually improve following treatment with somatostatin analogues.
    • Relative youth actually reflects a better prognosis.
    • Cardiac lesions are not reversible with treatment, deteriorate with time and frequently require replacement.
    • Patients with carcinoid heart disease,,,most die of progressive right heart failure within one year after onset of symptoms.
    • The prognosis of patients with recognised carcinoid heart disease has improved over the past two decades [and] may be related to valve replacement surgery
    Digoxin Toxicity Indications for administration of Digoxin specific Fab Fragment are:
    o haemodynamic instability
    o life-threatening arrhythmias
    o serum potassium >5 mmol/l in acute toxicity
    o plasma digoxin level >13nmol/l
    o ingestion of more than 10 mg digoxin in adults and 4 mg in children

    Deep venous thrombosis
    • Thrombosis involving the popliteal veins are considered to be proximal DVT, while thrombosis involving veins distal to popliteal veins are considered distal.
    • Anticoagulation for distal DVT is controversial as the incidence of pulmonary embolism in such a setting is very low. However, patients with distal DVT should be followed by serial Doppler studies, if not anticoagulated, because proximal extension of thrombosis can occur.
    Clopidogrel causing thrombotic thrombocytopenic purpura
    • fever, altered mental status, hemiparesis, anaemia, thrombocytopenia and renal impairment
    • This disorder can occur in less than 1% of patients receiving clopidogrel or ticlodipine.
    • The peripheral blood smear reveals fragmented RBCs (schistocytes, eg, spherocytes, segmented RBCs, burr cells, or helmet cells).
    • While further imaging with MRI would certainly be indicated, cerebral angiography would not be performed here as a next step, and in any case the low platelet count would give cause for caution with invasive procedures including lumbar puncture.



    Hyperlipidemia
    dysbetalipoproteinaemia (type III hyperlipoproteinaemia)
    • Palmar xanthomas are pathognomonic
    • It is caused by mutation in apoprotein E,
    • transmitted as an autosomal recessive trait
    • usually requires a secondary exacerbating metabolic factor for expression of the phenotype.
    • Therefore, secondary causes of hyperlipidaemia such as
    o hypothyroidism,
    o obesity,
    o diabetes mellitus,
    o renal insufficiency,
    o high-calorie,
    o high-fat diet or
    o alcohol are often encountered at diagnosis,
    • Patients are predisposed to peripheral vascular disease and coronary artery disease.
    • Lipid profile in these patients reveals
    o elevated cholesterol and triglycerides while high-density lipoprotein (HDL) is normal and low-density lipoprotein(LDL) low.
    o Definitive diagnosis can be made by lipoprotein electrophoresis or genotyping of apoprotein E.
    • Treatment involves
    o management of secondary causes

    Atrial septal defect should be closed if there is evidence of a
    • left-to-right shunt with a pulmonary flow to systemic flow ratio that is greater than or equal to 1.5:1.0,
    • volume overload of right-sided cardiac chambers, or
    • symptoms related to the defect.
    Atrial septal defect with atrial fibrillation
    • The patient should be cardioverted to sinus rhythm prior to any intervention to close the atrial septal defect.
    • A transoesophageal echocardiogram can give sufficient anatomical data as to the size and site of the defect.
    • It is well worth patients undergoing electrophysiological studies prior to any closure procedure. Any abnormal pathways predisposing to atrial flutter , fibrillation should be considered for radiofrequency ablation which can be curative.
    Cardiac transplantation

    Coronary artery disease (transplant vasculopathy) increases in frequency with time after cardiac transplantation and is present in almost half of all patients by 5 years after transplantation.
    • coronary artery disease in a cardiac transplant patient often presents atypically and may manifest with
     new-onset heart failure symptoms,
     decreased exercise tolerance,
     syncope (usually due to arrhythmias or conduction defects), or
     cardiac arrest.
    • Because transplant-related coronary artery disease is frequently asymptomatic or manifests with very atypical symptoms, regular screening with coronary angiography and/or noninvasive stress testing is generally performed,
    • Traditional risk factors
     hypertension,
     diabetes mellitus,
     dyslipidemia,
     smoking
     immunologic factors
    • Because the pathophysiology is a diffuse intimal thickening, standard revascularization methods are frequently not feasible.
    • There is evidence that statins help prevent and retard progression of transplant vasculopathy.
    • Prognosis is poor once significant transplant vasculopathy becomes symptomatic, and in appropriate candidates, another cardiac transplantation is a possible treatment option.

    Side effects for cyclosporine include
    o hypertension,
    o nephrotoxicity,
    o hypertriglyceridemia,
    o hirsutism,
    o gingival hyperplasia, and
    o tremor.
    o High levels of cyclosporine can cause seizures

    β-blockers and pregnancy
    • All available β-blockers cross the placenta and are present in human breast milk, resulting in significant levels in the fetus or newborn.
    • Therefore, when used during pregnancy, fetal and newborn heart rate and blood glucose monitoring are indicated.
    • Adverse fetal effects, have been associated with the use of atenolol, especially when initiated early in the pregnancy.
    o low birth weight,
    o early delivery, and
    o small size for gestational age
    o The World Health Organization considers atenolol (U.S. Food and Drug Administration [FDA] pregnancy risk category D) unsafe during breastfeeding as it concentrates in breast milk, resulting in a significant dose to the breast-fed infant with associated risks for hypoglycemia and bradycardia.
    o Metoprolol (pregnancy risk category C) should be considered as an alternative.

    Digoxin in pregnancy
    • risk category C drug.
    • Although it readily passes to the fetal circulation, no teratogenic effect has been reported in humans.
    • Digoxin is often used as a maintenance medication in patients with heart failure or atrial arrhythmias during pregnancy.
    • The indications for digoxin are identical to those for nonpregnant patients with heart failure.
    • It is recommended for patients with New York Heart Association class III heart failure to improve symptoms and reduce hospitalization.
    • It is not indicated in asymptomatic patient.

    Diuretics in pregnancy
    • Diuretics impair uterine blood flow and placental perfusion.
    • Continuation of diuretic therapy initiated before conception does not seem to have unfavorable effects.
    • Maternal use of furosemide during pregnancy has not been associated with toxic or teratogenic effects, although metabolic complications have been observed.
    • Neonatal hyponatremia and fetal hyperuricemia have been reported.
    • Use of diuretics should be limited to the treatment of symptomatic heart failure with clear evidence of elevated central venous pressure.
    • Furosemide (pregnancy risk category C)

    Central Retinal Vein Occlusion
    • Patients usually present with painless loss of vision
    • diffuse retinal hemorrhages in all four quadrants of the retina
    • as well as dilated, tortuous veins.
    • cotton-wool spots,
    • disc edema,
    • optociliary shunt vessels
    • neovessels might also be present.
    • Multiple etiologies should be considered including:
    o hypertension,
    o glaucoma,
    o optic disc edema,
    o hypercoagulable states,
    o vasculitis,
    o drug-induced, and
    o retrobulbar compression by tumors or grave's opthalmopathy

    left Subclavian steal syndrome
    • left upper extremity claudication precipitated by exertion
    • Examination findings include the
    o low blood pressure in the left arm compared with the right,
    o the diminished left radial and brachial pulses, and
    o the systolic murmur in the left clavicular region.
    • Another possible symptom is syncope or near-syncope due to subclavian steal syndrome, which occurs in the setting of significant stenosis of the subclavian artery and retrograde flow in the ipsilateral vertebral artery during upper extremity exertion.

    Transient ischemic attack in complex ascending aortic atheromas.
    • The presence of an ascending aortic atheroma of 4 mm or greater in diameter increases the risk of recurrent stroke.
    • Treatment either warfarin or antiplatelet

    Lyme carditis
    • is manifested by acute-onset, high-grade atrioventricular conduction defects that may occasionally be associated with myocarditis.
    • Carditis occurs in 5% to 10% of patients with Lyme disease, usually within a few weeks to months after infection.
    • Cardiac involvement can occur in isolation or with other symptoms of the disease.
    • Atrioventricular block can present in any degree, and progression to complete heart block is often rapid.
    • Atrioventricular block is usually within the node, but sinoatrial and His-Purkinje involvement have also been described.
    • Prognosis is good, with usual resolution of atrioventricular block within days to weeks.
    • In some patients, heart block is the first and only manifestation of Lyme disease, but the diagnosis can be confirmed by a positive IgM and IgG antibody response to B. burgdorferi. Lyme serologic testing should be considered in any patient with unexplained high-grade atrioventricular block, particularly in patients with potential tick exposure living in endemic areas.
    • Electrophysiology study is not indicated, since it does not provide additional prognostic information.
    • The preferred antibiotic regimen is intravenous ceftriaxone until the heart block resolves, followed by a 21-day course of oral therapy.
    • Erythromycin is considered a third-line agent for the treatment of Lyme disease, as it is less effective than penicillin or cephalosporin drugs. However, oral erythromycin can be used for patients with erythema migrans who are intolerant of amoxicillin, doxycycline, and cefuroxime.
    • Most cases of Lyme carditis resolve spontaneously, and neither temporary nor permanent pacemaker therapy is needed.
    • Temporary pacing would be required if the patient were hemodynamically unstable with bradycardia. However, this rarely occurs in the setting of Lyme carditis.
    • Indications for permanent pacemaker placement would include persistent high-grade atrioventricular block.

    Tetralogy of Fallot
    • Women with tetralogy of Fallot have an increased risk of having offspring with congenital anomalies.
    • Approximately 15% of women with tetralogy of Fallot have chromosome 22q11.2 microdeletion "DiGeorge Syndrome", which raises the risk of having a child with congenital heart disease substantially, from 4% to 6% in affected women without the microdeletion to approximately 50% in those with the microdeletion.



    Peripheral arterial disease

    • A supervised program of regular, repeated exercise to the point of near-maximal pain significantly increases pain-free walking time and walking distance in patients with symptomatic peripheral arterial disease.
    • In patients with class I acute limb ischemia (moderate to severe claudication but no rest pain, audible venous and arterial Doppler signals),
    o antiplatelet therapy along with systemic anticoagulation with heparin is indicated.
    • Patients with transient sensory deficits and no motor weakness are typically considered for intra-arterial thrombolytic therapy.
    • Patient with marked motor and sensory deficits; needs emergency surgical revascularization.
    • Patients with anesthesia, paralysis, and loss of vascular flow signals have irreversible ischemia and prompt amputation is required.
    • Patients with less dense sensorimotor defects and intact venous flow signals may obtain limb salvage, but only with immediate revascularization.
    • Patients without sensorimotor loss and with evidence of intact vascular flow are more likely to obtain limb salvage, but only with prompt vascular intervention.

    Traveler venous thrombosis
    • There is no evidence for an association between dehydration and travel-associated VTE and so whilst maintaining good hydration is unlikely to be harmful it cannot be strongly recommended for prevention of thrombosis
    • Travellers at the highest risk of travel-related thrombosis undertaking journeys of greater than 3 hours should wear well fitted below knee compression
  16. lolos

    lolos Guest

    i failed it is okay need to do more revision
    dr barwari you are a descent man and respectable man thank u for the notes god bless u and all this forum
  17. Dr Hopeful

    Dr Hopeful Guest

    YOU ROCK DR ALBARWARI


    May Allah give you reward for this
  18. caashif

    caashif Guest

    bravo!!!!!
    Al barwari that will really help
    May Allah help you in every walk of life
    Amin
  19. Dr albarwari

    Dr albarwari Guest

    Dear all
    ALSALAMUALAIKUM

    Regarding my notes,,,,,,,,,I copied them from pastest onexam sometimes guidelines otherwebsites,,,,,I recommend every one to have his or her own notes and this not substitute doing BOF and I did not comment or put those topics where I had good knowlege and informations for examplle atrial myxoma for me easy subject so I put very short notes on it while other subject may had taken longer

    Do not forget to do BOF as much as you can with making your own notes in the way to be easy understandable for you not me

    Abdulkhalik
    Zakho
  20. Dr albarwari

    Dr albarwari Guest

    Diabetes

    Recommended goals for management of adults with diabetes are
    • hemoglobin A1C <7.0%,
    • preprandial plasma glucose 90-130 mg/dL (5-7.22 mmol/L),
    • peak (2 hour) postprandial plasma glucose <180 mg/dL (9.99 mmol/L),
    • blood pressure <130/80 mm Hg,
    • triglycerides <150 mg/dL (1.69 mmol/L),
    • HDL cholesterol >40 mg/dL (1.03 mmol/L), and
    • LDL cholesterol <100 mg/dL (2.59 mmol/L).
    Pathology
    Compared with subjects with normoglycaemia, beta cell mass is reduced
    • By 50% in subjects with impaired fasting glucose
    • By 65% in subjects with Type 2 diabetes and
    • Over 90% in subjects with type 1 diabetes.
    The suggestion therefore is one of gradual insulin deficiency associated with increasing insulin resistance.
    Gestational diabetes mellitus
    • Patients with gestational diabetes mellitus have a 50% risk of developing type 2 diabetes mellitus in the 5 to 10 years after the diagnosis of gestational diabetes.

    Maturity onset of diabetes of youth
    • MODY3 due to
    o HNF1-alpha mutation (Hepatic nuclear factor1).
    o MODY3 is the cause of 2% of type 2 diabetes and makes up around 70% of MODY cases.
    o It presents most commonly in early adulthood and is associated with severe hyperglycaemia in some cases and frequent microvascular complications.
    o One-third of patients require insulin therapy and around
    o one-third may be controlled on oral hypoglycaemic drugs.
    o Sulphonylureas would be the initial oral therapy of choice.
    o It is linked to a mutation on chromosome 12q24, which is the cause of the HNF1-alpha mutation.
    • Next commonest MODY variant is MODY 2,
    o results from a glucokinase mutation leading to altered glucose sensing in pancreatic beta cells.
    o In contrast, 90% of MODY2 patients are controlled on diet therapy alone.

    Cellulites
    • Group B "not A" Streptococcus the commonest cause of cellulites in diabetics
    Diabetic ketoacidosis
    • Patients with diabetic ketoacidosis (DKA) are at increased risk of venous thromboembolism because of volume depletion, hyperglycaemia and their decreased conscious level.
    • As such standard prophylaxis against deep vein thrombosis is an important component of management.
    • Whilst phosphate depletion may be a feature of DKA, IV phosphate replacement is not part of routine management.
    • Sodium bicarbonate is also not used routinely and is only recommended in severe acidosis or circulatory collapse as an adjunct to insulin and fluid resuscitation
    Hyperglycaemic hyperosmolar state
    • occurs in older type 2 diabetic patients, some residual insulin production preventing the development of ketoacidosis, which occurs in type 1 diabetic patients more commonly.
    • pH normal
    • Serum urea elevated
    • Consequent on the osmotic diuresis due to hyperglycaemia, the patient will be
    o very dehydrated.
    o Hypotension
    o Serum sodium elevated
    • The initial goal is repletion of extracellular volume. 1-3 litres of normal saline will start to restore this
    • Then treat hypernatraemia, 0.45% saline is then given which replaces intra- and extracellular fluid loss,
    • 5% dextrose should be added when blood glucose reaches 15 mmol/l.


    Intensive glycemic control in the ICU
    • intensive glucose control increased mortality among adults in the ICU: a blood glucose target of 180 mg or less resulted in lower mortality than did a target of 81 to 108 mg
    • glucose levels between 140 and 180 mg/dL (7.8 and 10.0 mmol/L) may be optimal
    • is best achieved in the intensive care unit with an intravenous insulin infusion.
    • If patient is ready for transfer to a general ward, patient should be transitioned to an injectable regimen involving long- or intermediate-acting and rapid-acting insulins. Oral agents can be restarted before discharge
    • Insulin glargine, the dosage of which is typically adjusted every 2 to 3 days until optimal glycemic control is achieved, cannot quickly guarantee adequate control during the 1 to 2 days that this patient is likely to be in the ICU.
    • Sliding scale, this approach to glycemic control is considered inadequate because insulin is provided only when hyperglycemia becomes established.
    Management of hyperglycemia in the hospital setting
    • Hospitalized patients frequently experience stress hyperglycemia because of counterregulatory hormonal surges, which frequently complicate an acute illness.
    • Therefore, the best next step in managing this patient’s mild hyperglycemia is to measure his fasting plasma glucose level (or perform an oral glucose tolerance test) several weeks after discharge.

    Diabetes and Cardiovascular diseases
    • Studies suggest that diabetes is a coronary artery disease equivalent, i.e. that cardiovascular risk associated with diabetes is similar to that of patients with established ischaemic heart disease (IHD).
    • Therefore evidence from CARDS, HPS, etc. indicates that subjects with diabetes should receive statin therapy as this significantly reduces cardiovascular events.
    • Fibrates are more effective on hypertriglyceridaemia
    • ezetimibe would be associated with an approximate 20% reduction in cholesterol and diet a paltry 10%.
    • Statins such as rosuvastatin may reduce cholesterol by as much as 60%.
    Diabetes mellitus and Heart failure
    • The insulin sensitizing drugs metformin and the thiazolidinediones are contraindicated in patients with advanced heart failure.

    Diabetes mellitus and Renal failure
    • Glycemic control improves spontaneously
    • Metformin is contraindicated in men with a serum creatinine level greater than 1.5 mg/dL (132.6 µmol/L) or women with a level greater than 1.4 mg/dL (123.8 µmol/L). When the glomerular filtration rate is reduced, circulating concentrations of metformin can accumulate, which increases the risk of lactic acidosis.
    • Sitagliptin, a dipeptidyl peptidase-IV (DPP-IV) inhibitor that is frequently used in patients with chronic kidney disease. Inhibiting the degradation of DPP-IV increases glucagon-like peptide-1 levels and thereby leads to increased insulin secretion and decreased glucagon secretion. sitagliptin does not cause hypoglycemia. Sitagliptin is metabolized in the liver but excreted largely unchanged in the urine, and the dosage needs to be reduced by 50% to 75% in patients with renal insufficiency.
    Diabetic nephropathy
    • develops in approximately 40% of patients with type 1 diabetes and in 5% to 40% of patients with type 2 diabetes.
    • Without intervention nephropathy is likely to deteriorate with the development of macroalbuminuria. In association with the latter, renal function declines about 10% per year, ending in end-stage renal disease.
    • Proven interventions in the treatment of nephropathy include ACE inhibitors, low dietary protein and improved glycaemic control.
    • The evidence for good glycaemic control in the treatment of microalbuminuria in patients with type 1 diabetes suggests no clear benefit [DCCT]).
    • However, meta-analyses of the effects of ACEi on the development of nephropathy in type 1 diabetics show an albumin excretion rate 50% lower at two years in treated versus untreated patients.
    • The evidence for a low protein diet exists for overt proteinuria but not microalbuminuria.
    Diabetic Retinopathy
    • Maculopathy
    o Recent UK studies have put the 4-year incidence of maculopathy in type 2 diabetes patients as high as 10.4%,
    o 75% of cases of maculopathy being type 2 diabetes related.
    o In type 1 diabetes maculopathy is named as the cause of blindness in 14% of patients.
    • Immediate ophthalmology referral is recommended for
    o proliferative retinopathy (presence of new vessels signifies a 40% risk of blindness within 2 years if untreated),
    o rubeosis iridis,
    o vitreous haemorrhage, and
    o advanced retinopathy with fibrosis and
    o retinal detachment.
    • Referral within 6 weeks is recommended for
    o preproliferative retinopathy,
    o maculopathy and for
    o any cause of deterioration of more than two Snellen chart lines in visual acuity,
    o although the presence of email technology means that a same day opinion should be obtained from the ophthalmologist.
    • Routine referral may be considered in some
    o cases for cataract surgery or
    o in those patients with non-proliferative retinopathy but who have a large amount of hard exudates and
    o circinate formation.

    Rubeosis iridis
    • ocular pain is due to raised intraocular pressure.
    • Causes include
    o Sickle cell disease
    o Diabetes mellitus
    o central retinal vein occlusion and
    o carotid artery occlusive disease.
    • Diagnosis is with fluorescein angiography to assess extent of retinal ischaemia and ultrasound.
    • Progression of rubeosis is thought to be reduced by aggressive management of the underlying medical cause and reduction of the area of viable retina with pan-retinal photocoagulation.
    • Topical steroids and standard treatments for open angle glaucoma are also of value.
    • Unfortunately prognosis for this condition is generally poor as many patients present at a late stage.

    Diabetic autonomic neuropathy
    • early satiety due to gastroparesis,
    • poor night vision due to pupillary dysfunction, and
    • urinary incontinence.

    Cardiovascular neuropathies
    • orthostatic hypotension,
    • absent normal variation of the heart rate with breathing,
    • tachycardia, and
    • sudden death.
    • Patients should thus undergo further testing, such as an exercise stress test, to exclude exercise-induced silent ischemia.
    • The treatment of orthostatic hypotension, fludrocortisone and midodrine ,,,,,Patients being treated with these drugs should be closely monitored for supine hypertension, abnormal potassium levels, and fluid retention.

    Postural hypotension
    • A standing BP of 110 systolic is clearly acceptable,
    • first step is in stopping diuretics and monitoring his blood pressure over the subsequent 2-4 weeks.
    • If he still has significant postural hypotension then the next steps would be to add elastic stockings, then
    • fludrocortisone.
    Neurogenic bladder
    • which can manifest as recurrent urinary tract infections and overflow incontinence.
    • Measuring postvoid urinary residual volumes or obtaining a bladder ultrasonogram will determine whether high urinary residual volumes are present.
    • If they are, prokinetic drugs (such as bethanechol chloride) can be given, or
    • an intermittent urinary self-catheterization regimen can be initiated.
    • Regular and complete bladder emptying will help reduce the incidence of urinary tract infection and possibly reverse or improve the patient’s renal insufficiency
    • Anticholinergic agents, such as oxybutynin, inhibit contraction of both the normal and unstable bladder. Oxybutynin is highly effective in the treatment of detrusor instability (overactive bladder). However, oxybutynin is contraindicated in patients with an atonic bladder and would likely exacerbate this patient’s problems.
    Neuropathic ulcer
    • commonly found on the pressure points of the feet and are painless.
    • Between 5 and 13% of patients have neuropathy at diagnosis of type-2 diabetes.
    • Ten per cent of people have absent dorsalis pedis pulses. Therefore, their absence does not indicate ischaemia.
    • Venous ulcers are usually found on the gaiter area of the ankle.
    • Ischaemic ulcers are found on the dorsa or edges of the feet. The feet are cold, pulseless, and hairless, and the nails are in poor condition.
    • Infected ulcers are malodorous and often exude pus.

    UTI and Diabetes
    • Candida urinary tract infections (UTIs) occur more commonly in uncontrolled diabetic patients.
    • An "Methicillin resistant Staphylococcal aureus" MRSA UTI occurs in patients with indwelling lines/prostheses.
    • Escherichia coli strains resistant to ciprofloxacin tend to be seen in elderly patients, especially those who live in nursing homes.
    Necrobiosis lipoidica diabeticorum.
    • Necrobiosis lipoidica is seen in 0.3–1% of patients with diabetes and is
    • more common in females.
    • Around 40–60% of patients with necrobiosis lipoidica have diabetes
    • presents in young adults or in early middle life.
    • may precede symptoms and signs of diabetes by several months " Urine dipstick is negative and a fasting blood glucose is normal"
    • The lesions are usually managed with
    o support bandaging
    o Treatments with topical steroids, injectable steroids, skin grafting and camouflage creams have been used as therapies.
    o low-dose aspirin or topical steroids.

    Diabetic amyotrophy
    • uncommon and disturbing condition which is said to usually affect men in their fifties who have type-2 diabetes.
    • weight loss, burning proximal muscle pain and weakness. quadriceps wasting.
    • The condition affects lumbar sacral plexus lower motor neurones.
    • Presentations may be :wasting of the quadriceps muscles bilaterally with loss of power. Loss of Knee and ankle jerks some loss of light touch and pinprick sensation over both feet and ankles. Plantar responses may be flexor or extensor.
    • EMG shows multifocal denervation in paraspinous and leg muscles.
    • Prior to making the diagnosis it is important to exclude other causes such as disc disease or malignancy "MRI spinal cord"
    • The aetiology of this condition is unknown, but oral antidiabetic agents may play a part. Transition to insulin therapy is therefore recommended, additionally in this case it would improve blood glucose control.
    • Recovery happens over 3–4 months, but only 50% achieve complete recovery. Partial or complete resolution occurs with control of hyperglycaemia
    •


    Insulinoma
    • best evaluate the patient for insulinoma, a prolonged fast (up to 72 hours) under strict medical observation is often necessary.
    • Serum glucose, insulin, C-peptide, and proinsulin levels are measured at 4- to 6-hour intervals throughout the supervised fast.
    • The fast is discontinued once the glucose value falls below 45 mg/dL (2.5 mmol/L) with associated symptoms of hypoglycemia and appropriate blood tests (measurement of plasma glucose, insulin, and C-peptide levels) are obtained.
    • More than 95% of patients with insulinoma will have hypoglycemia within 72 hours.
    • Insulin and C-peptide levels will generally be elevated, as will the proinsulin level, which suggests a greater tumor release of immature insulin.
    • Once the diagnosis of insulinoma is confirmed biochemically, imaging studies of the pancreas are obtained, beginning with an abdominal CT scan

    Charcot’s arthropathy
    • indium labelled white cell scan is the best way to differentiate between infective causes and Charcot’s arthropathy.
    • Charcot’s is thought to occur due to increased blood flow as a result of neuropathy. This results in increased osteoclast activity and bone turnover; the foot is then susceptible to often very minor trauma and destructive changes take place.
    • joint immobilisation for at least 3 months in an aircast type non-weight-bearing plaster. This is to allow bone remodelling/repair to occur.
    • Bisphosphonates are a useful adjunct to the healing process as they reduce osteoclast activity.
    • Whilst insulin therapy is likely to improve glycaemic control and slow further progression of neuropathy, it will not affect recovery of the Charcot’s joint.




    High dose metformin is thought to interfere with the enterohepatic circulation of bile salts, leading to reduced reabsorption of bile salts from the ilieum


    Hyperlipidemia
    • The mode of action of fibrates is to
    o enhance lipoprotein lipase activity,
    o increase low-density lipoprotein (LDL) receptor-mediated clearance of LDL and
    o increase high-density lipoprotein (HDL) synthesis.
    o This leads to a corresponding fall in triglycerides due to a fall in very low-density lipoprotein (VLDL), and a rise in HDL.
    o In total, they reduce triglycerides by 20-60%, LDL by 5-25%, and increase HDL by 15-30%.
  21. Shez

    Shez Guest

    anyone else with me 4 paces....

    my exam is 10th june in inverness, scotland............ i am uk graduate
  22. part2doc

    part2doc Guest

    to april recall

    to april recall:

    Where are you?

    Did you pass?

    I pray that you passed.
  23. Drcool

    Drcool Guest

    Sarahpart2mrcp, where r u located? Wat are your plans for paces?
  24. OKO

    OKO Guest

    Dear dr Barwari , Can you collect all the files you have and

    upload it to one website like mediafire or hotfile

    i think that will be right so as not to disrupt the notes
  25. RNA

    RNA Guest

    HI

    DERA ALBARAWI...keep the good work going...really in need of ur notes..v tough duty hrs..failed twice....if u can send ur notes to me..i shall be extemely happy....my id..drowaiskhanATgmailDOTcom.....waiting anxiously
  26. RNA

    RNA Guest

    DEAREST ALBARWARI....IF IT IS NOT POSSIBLE FOR U TO SEND EVERY 1 NOTES...KINDLY UPLOAD UR NOTES ON THIS V FORUM TILL END..PL PL PL DONT LEAVE US BEHIND...MAY ALLAH HELP U IN PACES
  27. oman

    oman Guest

    dr albarwari dr right answes

    any idea about books and online cources for paces
    how to prepare
    when to appear
    iam planning for 2012 1st diet
  28. any body for november
  29. drjim

    drjim Guest

    yaa,i am planning in nov......india,
  30. drjim

    drjim Guest

    dear dr.oman , albarwari ,and others ...i am planning to giv paces in nov at chenni,pls suggest me best online courses,books for paces...i hav 2 start as early as possible..bcoz i wont get much free time...iam a consultant physician in india,running a busy clinic and working in teaching hospital.....so i wont be getting sufficient time to prepare towards end...if u get any information pls help me.may ALLAH bless all of us.
  31. choroo

    choroo Guest

    consultant giving MRCP
  32. Kumar Mongar

    Kumar Mongar Guest

    Thank you Dr Albarwari for your notes. Please upload more. Thank againg.
  33. Dr albarwari

    Dr albarwari Guest

    thanks for all colleagues who comment on the notes,,,,,

    I received an email from a GUY named "Dr warning" say this notes are illegal???? any how I shall post more

    Dear OMAN
    I am happy to hear you again really I do not have much lnformations about PACES
    I do not know where to sit PACES as I said previosly I have difficulty in getting VISA ,,,,,shall I ask the colleague from INDIA is it possible for me to sit PACES in INDIA
  34. Dr albarwari

    Dr albarwari Guest

    Endocrinology


    Diabetes insipidus
    Osmolality, plasma 275-295 mosm/kg
    Initial plasma osmolarity Initial urine osmolarity Water deprivation urine Desmopressin urine
    Normal 275-295 600 > 600 > 600
    Nephrogenic DI >295 <300 No effect <300 No effect <300
    Cranial DI >295 <300 No effect <300 > 600
    Partial cranial DI >295 <300 300-400 400-600
    Psychogenic <275 <300 300-400 400
    • If initial urine osmolarity >660 it exclude DI
    • Psychogenic Both the plasma and urine osmolalities are low
    • During pregnancy sNa and plasma osmolarity are in lower normal level,,,,so DI can easily be missed in pregnancy so finding Na and osmolarity in upper normal level is abnormal high
    Desmopressin
    • can cause hyponatremia if a person continues to drink without any fluid restriction, particularly if their fluid intake is excessive
    • In patients receiving desmopressin who develop severe hyponatremia and a low urine output, cortisol deficiency should be part of the differential diagnosis.
    Cortisol is necessary for the distal nephron to excrete a water load. Thus, cortisol deficiency may mask diabetes insipidus.

    Cerebral salt wasting a syndrome characterized by hypovolemia and hyponatremia, usually occurs within 10 days of a neurosurgical procedure or disease, particularly subarachnoid hemorrhage.

    Hypopituitarism
    • is a common late finding after irradiation of pituitary adenomas. radiation therapy typically does not cause damage to the posterior pituitary
    • In patients with panhypopituitarism, cortisol should be replaced before other hormones
    Post-traumatic Hypopituitarism
    • a frequency of hypopituitarism in up to 35% to 50% of patients after a motor vehicle accident or subarachnoid hemorrhage.
    • The most important hormonal axis to test is the hypothalamic-pituitary-adrenal axis, and an 8 AM serum cortisol measurement is the best first test to determine deficiency of this axis.
    • If the basal cortisol level is equivocal (that is, between 6 and 18 µg/dL [166 and 497 nmol/L]), then testing with low-dose (1 µg) cosyntropin stimulation may prove valuable.
    • Assessment of the other pituitary axes should eventually be carried out in this patient, but the results of these tests are not as potentially lifesaving as (and thus are less critical than) the results of an early morning measurement of the serum cortisol level.
    • Growth hormone would be the last hormone assessed once all other deficits have been tested for and corrected.
    • If there are three or more pituitary hormonal axes found to be deficient, a low insulin-like growth factor I level would establish a diagnosis of growth hormone deficiency.
    • Symptoms of tiredness, poor concentration and weight gain suggest growth hormone (GH) deficiency and this is supported by the lowish IGF-1 concentration.
    • The diagnosis of secondary hypogonadism is established if a patient’s testosterone concentration and sperm count are low and serum luteinizing hormone and follicle stimulating hormone levels are inappropriately normal or low.
    • A serum free thyroxine (T4) level will indicate thyroid hormone status more accurately than measurement of the serum thyroid-stimulating hormone level
    Prolactinoma
    • Prolactin more than 6000 in macroadenoma
    • Always consider the possibility of pregnancy in reproductive-aged females, because this is the most common cause of secondary amenorrhea
    • hypoestrogenism include vaginal dryness, dyspareunia, and a decline in bone mineral density (ie, osteopenia or osteoporosis).
    • Dopamine agonists are preferred initial treatment because of their very high efficacy.
    • Radiation therapy is rarely performed for prolactinomas because of the high efficacy rates of dopamine agonists.
    • Somatostatin analogues have not been shown to have substantial prolactin-lowering or tumor-shrinking effects in patients with prolactinomas
    • surgery is reserved for the few patients who cannot tolerate or respond to dopamine agonists.
    • optic nerve compression gives no time to wait. In this situation, dopamine agonists may be used as an adjunct to surgery.
    • Severe hypogonadism in a young male with an elevated serum prolactin level strongly suggests pituitary macroadenoma
    • In men with massive prolactinomas, irreversible damage to the gonadal axis may occur that necessitates testosterone replacement therapy, despite normalization of the prolactin level.
    Women with microadenomas
    • The dopamine agonist bromocriptine has been shown to restore ovulatory cycles in greater than 80% of women.
    • A dopamine agonist would be indicated if pregnancy were desired.
    • Amenorrhea, which implies hypo-estrogenemia and an increased risk for osteoporosis. Oral contraceptives will supply needed estrogen and, at the same time, provide contraception if patient not interested in becoming pregnant
    • oral contraceptive use is safe in women with microadenomas, and there is minimal risk of tumor enlargement.
    • For women with prolactinomas, dopamine agonists are stopped once pregnancy is achieved. There are no documented risks of fetal malformations or other adverse pregnancy outcomes for these agents
    • Symptomatic growth occurs in approximately 30% of macroprolactinomas and 3% of microprolactinomas in the second or third trimester, which necessitates reinstitution of the dopamine agonist, transsphenoidal surgical decompression, or delivery if the pregnancy is sufficiently advanced
    Nonfunctioning pituitary tumors
    • The increase in prolactin levels due to the hypothalamic or stalk dysfunction
    • The most appropriate treatment for such an adenoma is surgery.
    • Nonsecreting adenomas generally do not enlarge and cause symptoms during pregnancy
    Prolactinoma "macroadenoma" during pregnancy
    • dopamine agonists are stopped once pregnancy is achieved.
    • Dopamine agonists are reinstituted when breast feeding is completed.
    • Approximately 30% of patients with macroprolactinomas will experience clinically significant enlargement of their prolactinomas during pregnancy.
    o If this occurs, options include reinstitution of dopamine agonists, surgery, or delivery, depending on fetal viability.
    • In contrast, only approximately 3% of women with microadenomas will experience such enlargement.
    • Tumor enlargement is due both to the elimination of the dopamine agonist that had been controlling tumor size and to the stimulatory effect of the high estrogen status of pregnancy.
    • Follow-up studies of women who became pregnant after using cabergoline or bromocriptine have shown no increased risk of fetal malformations, premature deliveries, or stillbirth. Therefore, the patient is unlikely to encounter any of these problems.
    Lymphocytic hypophysitis during pregnancy
    • a pituitary mass that mimics an adenoma is typically seen on an MRI.
    • Diffuse enhancement of a symmetrically enlarged pituitary gland on MRI is also characteristic.
    • This disorder, which usually develops intrapartum, is a destructive process thought to have an autoimmune basis.
    • Adrenocorticotropic hormone (ACTH) deficiency occurs in 65% of patients with such lesions and is a major cause of death
    • Thyroid-stimulating hormone deficiency occurs in 60% of patients with this disorder, and other hormonal deficits are of lower frequency.
    • The only way to diagnose the lesions of lymphocytic hypophysitis with certainty is by biopsy,
    • the size of most lesions decreases after delivery.
    • Serial visual field testing is indicated. If field defects do develop, surgical debulking may be necessary.

    Craniopharyngioma
    • headache (55-86%),
    • endocrine dysfunction (66-90%)
    o A moderately elevated prolactin up to 3000
    o 40% of patients have symptoms of hypothyroidism
    o 25% of patients have symptoms of adrenal failure
    o 20% have diabetes insipidus (eg, excessive fluid intake and urination).
    o 8%of adults complain of decreased sexual drive
    o 90% of men complain of impotence, while most women complain of amenorrhea.
    o Most young patients present with growth failure and delayed puberty.
    • visual disturbances (37-68%)
    o Optic pathway dysfunction on presentation is noted in 40-70%
    • Other manifestations hyperphagia and obesity, psychomotor retardation, emotional immaturity, apathy, short-term memory deficits, incontinence).
    • Short stature is present in 23-45% and obesity in 11-18%.
    • Three major clinical syndromes have been described and relate to the anatomic location of the craniopharyngioma.
    o Prechiasmal localization typically results in associated findings of optic atrophy (eg, progressive decline of visual acuity and constriction of visual fields).
    o Retrochiasmal location commonly is associated with hydrocephalus with signs of increased intracranial pressure (eg, papilledema, horizontal double vision).
    o Intrasellar craniopharyngioma usually manifests with headache and endocrinopathy




    Craniopharyngiomas during pregnancy
    • less common than adenomas
    • An MRI would typically show an irregular cystic lesion with an enhancing wall, not the symmetric sellar lesion
    • Craniopharyngiomas also cause panhypopituitarism and diabetes insipidus
    Acromegaly
    • Acromegaly can be diagnosed by demonstrating an elevated insulin-like growth factor 1 level in a patient in whom there is clinical suspicion of the disorder.
    • Transsphenoidal surgical resection is typically the treatment of choice.
    • In patients with pituitary tumors who are not cured by surgery, hormone levels often normalize with use of somatostatin analogues.such as octreotide or lanreotide. These drugs can normalize GH and IGF-1 levels in approximately 50% of patients when given adjunctively after pituitary surgery. They also commonly decrease tumor size.
    • Cabergoline normalizes GH and IGF-1 levels in only 10% to 20% of patients.
    • When transsphenoidal surgery is unable to cure a patient with a pituitary tumor, a second surgery, such as craniotomy, does so in only approximately 25% of patients. Because craniotomy also has substantial morbidity, it would rarely be used in a patient such as this one.
    • Radiation therapy may normalize GH and IGF-1 levels, but only after an extended period of time. With conventional radiation therapy, hormone levels in approximately two thirds of patients normalize in approximately 10 years; with gamma knife stereotactic radiation therapy, the time is reduced to 4 years. Neither type of radiation therapy would have a normalizing effect on these levels within 1 year.

    McCune–Albright syndrome
    • due to a mutation in a G-protein.
    • café-au-lait spots and
    • endocrinopathies. thyrotoxicosis
    • There is an increased risk of osteosarcoma and other connective tissue tumours,
    • precocious puberty the patient is at increased risk of developing breast carcinoma.
    Hyperthyroidism
    • the finding of an inappropriately normal level of thyroid-stimulating hormone suggests a pituitary cause of the hyperthyroidism. patient should undergo MRI of the pituitary gland to detect a possible thyroid-stimulating hormone (TSH)– secreting tumor.
    • Factitious thyrotoxicosis show undetectable thyroglobulin
    • IV heparin interferes with the thyroid function tests assay on occasions displacing bound thyroid hormone.
    • Long-term remission following antithyroid drugs is of the order of 15%, with the vast majority relapsing. Thus, frequently, radio-iodine is advocated as a primary treatment - particularly for multi-nodular or toxic solitary nodules. However, approximately 80% will have long-term hypothyroidism following radio-iodine.
    • There is no evidence of increased risk of thyroid neoplasia or gastric neoplasia following radioactive iodine (RAI).
    • Goitre shrinkage may occur in up to 30% following RAI.


    Thyrotoxicosis in patient receiving Digoxin need to increase digoxin dose
    Anticoagulated patients developing thyrotoxicosis require Decrease warfarin dose,


    Agranulocytosis with carbimazole
    • less than 1% of cases and
    • sore throats are very common.
    • It is not uncommon to see a drop in WCC associated with thionamides, if WBC and neutrophil counts are normal OR just below normal, the carbimazole continued.
    Thyroid storm
    • require hospital admission to an intensive care unit.
    • Fever is the most characteristic feature, with the temperature often rising above 41آ°C.
    • There may be evidence of organ damage
    • ECG show a fast AF
    • Appropriate therapy includes a combination of
    o β-blockers, propranolol (240-480 mg/d)
    o antithyroidal medications, propylthiouracil (>450 mg/d)
    o saturated sodium potassium iodide plus
    o hydrocortisone therapy,
    o cooling of body temperature, and
    o treatment of any underlying precipitant "chest infection"
    • Propranolol and propylthiouracil have the added benefit over atenolol and methimazole of reducing T4 to T3 conversion.
    Graves disease and ophthalmopathy
    • Graves disease is complicated by Graves ophthalmopathy in approximately 5% to 10% of patients.
    • Graves ophthalmopathy is an autoimmune disease of the retro-orbital tissues that may present with proptosis and periorbital edema.
    • Patients may report irritation in the eyes, tearing, ocular pain, and changes in vision. Vision loss may occur.
    • A persistent thyrotoxic or hypothyroid state appears to exacerbate eye disease activity, so patients should be made euthyroid as soon as possible.
    • Radioactive iodine should be avoided as treatment in patients with significant thyroid-associated eye disease but can be used in patients with mild ophthalmopathy if concomitant prednisone therapy is used.
    • Orbital decompression surgery is reserved for patients with severe ophthalmopathy that has not responded to medical treatment.
    Hashimoto disease
    • Patients with Hashimoto disease can have normal thyroid hormone levels but are at increased risk for hypothyroidism in the future,,so patient should have annual thyroid function tests.
    Myxoedema coma
    • If associated hypoadrenalism is suspected the immediate management is Hydrocortisone
    • If NO hypoadrenalism is suspected the immediate management is IV thyroid hormone - either T4 or T3

    Secondary hypothyroidism
    • The best way to diagnose central hypothyroidism is by measuring the level of the peripheral hormone T4. Similarly, thyroid hormone treatment is monitored and adjusted by measuring free T4 rather than TSH levels.
    • Progressive loss of pituitary hormones is to be expected after pituitary irradiation ,,,,fatigue and constipation and a recent elevated LDL-cholesterol level
    Hypothyroidism while on lithium
    Patients who develop hypothyroidism while on lithium therapy may require levothyroxine therapy. Because the patient’s bipolar disorder has been well controlled on his present regimen, the lithium should not be discontinued.
    Euthyroid sick syndrome,
    • particularly common in patients with chronic renal failure
    • small reductions in both free T3 and free T4 and normal or suppressed TSH
    • abnormal results on thyroid function tests that often normalize after recovery; This should have repeat thyroid function tests in 4 to 8 weeks.
    • neither levothyroxine nor liothyronine is indicated for treatment of the thyroid function changes seen with such non thyroidal illness.
    Thyroid nodule
    • Fine-needle aspiration is the mainstay in the evaluation of such thyroid nodules in euthyroid patients and has an excellent sensitivity and specificity for detecting cancer.
    • Ultrasonography is superior to CT in the evaluation of thyroid nodules, except when there is a goiter with substantial substernal extension.
    • Thyroid scanning has no role in the initial workup of thyroid nodules because both benign and malignant nodules tend to be hypofunctional or “cold†on a thyroid scan.
    • Thyroid scanning may be helpful when the thyroid-stimulating hormone (TSH) level is suppressed to assess for a hyperfunctioning (“hotâ€) nodule that does not require fine-needle aspiration biopsy. Hyperfunctioning nodules are rarely malignant.

    Thyroid cancer
    • nodule which is 'cold' on uptake scanning
    • Thyroid-stimulating hormone suppression by levothyroxine is the standard of care in patients who have thyroid cancer, with the degree of suppression determined by the severity of disease
    • TSH suppression has shown benefit is reducing thyroid cancer recurrence. Typically, patients with low-risk stage I and II disease have a target TSH level in the low-normal to just-below-normal range (0.3 mU/L)
    • Thyroid cancer associated with Graves' disease is not uncommon and usually due to papillary carcinoma and must be considered in suspicious/expanding nodules
    Amiodarone-induced thyrotoxicosis
    • Amiodarone which inhibits the peripheral conversion of thyroxine (T4) to tri-iodothyronine (T3) so consequently T4 may be elevated and T3 low
    • Radioiodine uptake scan disting between amiodarone induced thyrotoxicosis type 1 or type 2
    • Type 1
    • normal radioiodine uptake
    • normal interleukin 6 (IL-6) levels.
    • amiodarone should be discontinued IF there is alternative
    • treated with a combination of antithyroid drugs and potassium perchlorate therapy
    • High-dose antithyroid drugs are needed to treat type 1 AIT as they have less effect due to the high iodine load.
    • Type 1 AIT should be treated when stable with either radioiodine therapy or thyroidectomy
    • Type 2
    • decreased radioiodine uptake on thyroid scan
    • raised IL-6 levels.
    • treated with a combination of antithyroid drugs and corticosteroids such as prednisolone
    • type 2 AIT may progress to hypothyroidism
    • The amiodarone need not necessarily be stopped if given for VT
    • Colour flow Doppler ultrasound can be used to differentiate the two. Blood flow is increased in type 1 and decreased in type 2.
    • Radioiodine is not usually effective due to reduced uptake by the thyroid due to high iodine levels.
    • In both cases, if amiodarone cannot be withdrawn then total thyroidectomy should be considered.

    Lithium would typically cause low T4 and elevated thyroid-stimulating hormone (TSH).
    Thyroglobulin autoantibodies are present in:
    • Grave's disease
    • Hashimoto's thyroiditis
    • idiopathic thyroid atrophy
    • De Quervain's thyroiditis - transiently
    • 7% of males, and 15-20% of females without thyroid disease
    Antithyroid peroxidase antibodies (previously known as thyroid microsome autoantibodies) are present at:
    • high titre, in:
    o Hashimoto's thyroiditis
    o idiopathic thyroid atrophy
    • low titre, in:
    o Grave's disease
    o De Quervain's thyroiditis
    o 8% of males, and 10% of females without thyroid disease
    High titres of thyroid autoantibodies, particularly to thyroid microsomes, is associated with increased likelihood of progress to myxoedema as it reflects increased damage to the thyroid cells


    Graves’ disease and ophthalmopathy
    • an initial inflammatory phase followed by a fibrotic stage.
    • If the symptoms are mild patients can be managed with lubricants and eye patches.
    • For active disease treatment, options include
    o orbital decompression,
    o orbital radiotherapy and
    o glucocorticoids.
    • There is concern that radio-iodine could exacerbate Graves’ ophthalmopathy.
    • Patients with pretibial myxoedema tend to have more severe ophthalmopathy.
    Secondary hyperthyroidism
    • elevated tri-iodothyronine (T3)
    • elevated thyroxine (T4)
    • normal TSH.
    • MRI head scan may be expected to demonstrate a pituitary macroadenoma.
    • Alpha subunit is also secreted in large amounts and measurement of this should yield an elevated alphaSU:TSH ratio (usually 1:1).
    • The diagnosis should be suspected when TSH concentrations are not suppressed in the presence of hyperthyroidism.

    Thyroid in pregnancy
    • It is a feature of normal pregnancy that T3 , T4 levels show a slight increase in the first trimester due to human chorionic gonadotrophin (HCG) stimulation.
    • TSH may be mildly suppressed in up to 13.5% of pregnancies during the first trimester, and this is considered a normal variant.
    • Thyroid-binding globulin has a twofold increase in concentration during pregnancy as a result of reduced hepatic clearance and increased synthesis under oestrogen stimulus.
    • Patient on oral contraceptive pill has high Total thyroxin because Oestrogen therapy is associated with elevation of thyroxine binding globulin in the serum,,, Thus the total serum thyroxine may be misleading in this case, and serum free thyroxine will confirm whether this patient is hypothyroid or euthyroid.

    Thyrotoxicosis in pregnancy
    • Thyrotoxicosis, of which 85% of cases are due to Graves' disease, there may be NO goiter
    • Toxic thyroid adenoma is responsible for a much smaller number of cases of thyrotoxicosis in pregnancy
    • propylthiouracil as the primary treatment for toxic thyroid adenoma in pregnancy.
    • Suppressed TSH with normal free thyroid hormones does not require intervention.
    • A block and replacement regime is contra-indicated as both carbimazole and propylthiouracil cross the placenta far better than thyroxine and so may induce fetal hypothyroidism.
    • If patient on carbimazole and become pregnant the patient should continue treatment with carbimazole
    • Both carbimazole at a suggested daily dose of 10–20 mg/d and propylthiouracil (PTU) at a dose of 150 mg bd are acceptable for use in pregnancy,
    • PTU may be more protein bound and so less is transmitted to the fetus, but compliance with carbimazole is generally better.
    • Importantly however there is some controversy that the azole drugs may be associated with fetal scalp defects, aplastic cutis, and oesophageal atresia.
    • In patients not controlled at maximal carbimazole, switching of antithyroid drugs may be appropriate;
    • In patients who have an adverse reaction to anti-thyroid drugs, poor compliance, or poor response despite high doses, subtotal thyroidectomy may be required, the second trimester being the preferred time for surgery.
    • Relapsed Graves' thyrotoxicosis,with history of previous thyrotoxicosis treated with anti-thyroid treatment and dysthyroid eye disease, which has now relapsed in pregnancy.The patient needs to be rendered euthyroid prior to any definitive therapy, so give propylthiouracil




    Postpregnancy thyrotoxicosis Graves' disease OR postpartum thyroiditis
    • Measurement of TSH-receptor autoantibodies, which are present in more than 90% of patients with Graves' disease but are not present in postpartum thyroiditis, can distinguish between the two disorders in a patient with postpregnancy thyrotoxicosis.
    • Anti-thyroid peroxidase antibodies will likely be positive in both disorders, and serum thyroglobulin levels are elevated in both disorders.
    • Radioiodine uptake will be low in thyroiditis and elevated in Graves' disease; however, radioiodine is secreted into breast milk, and the isotope most commonly used to measure radioiodine uptake (131I) has such a prolonged duration of activity that further breastfeeding is stopped.
    • Antithyroid drugs are better reserved for confirmed Graves' disease

    Hypothyroidism in pregnancy
    • In patients already on thyroxine when they become pregnant, thyroid function tests should be assessed at 6–8 weeks’ gestation and then at 16–20 and 28–32 weeks.
    • Average increase in thyroxine requirements is 25–50 μg and the increased need for thyroxine ceases immediately after delivery.
    • In patients with positive thyroid autoantibodies there is a twofold increased risk of spontaneous abortion.
    • In patients who are suboptimally treated for hypothyroidism there is a 21% risk of pregnancy-induced hypertension.
    • Maternal hypothyroidism is also associated with increased risk of pregnancy induced anaemia and postpartum haemorrhage.

    Hypothyroidism in pregnancy
    • Because a fetus depends on maternal thyroid hormone for the first 10 to 12 weeks of gestation, the thyroid levels of pregnant women with hypothyroidism should be carefully monitored.
    • because standard free T4 levels are not as accurate in pregnant patients. The total T4 level should be kept stable at approximately 1.5 times the normal range, and
    • the TSH level should be kept in the lower range of normal.
    • Because of estrogen elevation during pregnancy, thyroid-binding globulin (TBG) levels increase. However, without an increase in the dosage of levothyroxine, free T4 levels may decrease as more T4 becomes bound by TBG. After delivery, TBG levels decrease, as do thyroid hormone requirements.
    • TSH level should be rechecked. If the TSH level is any higher now, an increase in the levothyroxine dosage is warranted.
    • Pregnant patients with hypothyroidism may require an increase in their levothyroxine dosage of approximately 35% to 50% as early as the first trimester. because undertreatment of maternal hypothyroidism can have a potentially negative effect on fetal neurocognitive development.
    • Measurement of the free triiodothyronine (T3) level is not useful in the evaluation of hypothyroidism because T3 levels typically remain within the reference range until the point of severe hypothyroidism. This pattern is unaltered by pregnancy.
    Subclinical hypothyroidism
    • Patients with subclinical hypothyroidism who have a serum TSH value above 10 µU/mL (10 mU/L) have been shown to have reductions in their LDL cholesterol concentrations when treated with levothyroxine
    Post-partum thyroiditis
    • develop some 3–7 months after pregnancy
    • 5–7% of women and in
    • 30–52% of cases anti-TPO antibodies are positive.
    • Permanent hypothyroidism is said to develop in around 40% of patients, the frequency is increased in patients with positive anti-TPO antibodies.
    • Standard treatment for postpartum hypothyroidism is low-dose thyroxine (around 50 μg), with a withdrawal period after 6 months to measure recovery of thyroid function.
    DeQuervain's or subacute thyroiditis
    • A radio-iodine uptake scan usually shows minimal or zero uptake.
    • The condition is treated with steroids and/or beta-blockers.


    Hypercalcaemia
    • Thyrotoxicosis
    o Mild hypercalcemia are found in approximately 10% of patients with thyrotoxicosis
    o suppressed parathyroid hormone levels.
    o Thyroid hormone has direct bone-resorbing properties that cause a high-turnover state; if left untreated, progression to osteoporosis often occurs.
    • Lithium
    o elevated level of PTH,
    o up to 10% become mildly hypercalcemic with PTH levels that are high normal or slightly elevated.
    • Serum calcium levels should be monitored in immobilized patients to check for the development of hypercalcemia of immobilization, which is more likely to occur in patients with high bone turnover, such as young patients and patients with Paget disease
    • Granulomatous diseases involves excess production of 1α-hydroxylase, which converts 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D; corticosteroid administration diminishes this hypercalcemia.
    • Malignancy is the most common cause of non-parathyroid hormone (PTH)–mediated hypercalcemia
    • Malignancy-associated hypercalcemia is differentiated into two forms:
    o local osteolytic occurs when tumor growth in the skeleton leads to the release of calcium by the stimulation of local cytokines ,,multiple myeloma, adenocarcinoma of the breast and certain lymphomas
    o Humoral hypercalcemia systemic effect of a circulating factor produced by neoplastic cells. PTH-related protein (PTHrP). squamous cell carcinomas, such as those of the lung, esophagus, or head and neck. PTHrP levels can be measured, but this is rarely needed to establish the diagnosis of humoral hypercalcemia of malignancy.
    • the first step management is aggressive volume expansion with intravenous normal saline
    • furosemide should no longer be recommended as part of the management of hypercalcemia.
    • Bisphosphonates lower the serum calcium level, with their maximum effect seen in 2 to 4 days. Their duration of effect is usually several weeks ,,,,Zoledronate appears to have the longest-lasting effect (1-1.5 months) and a faster onset of action than other bisphosphonates; it is approved for use in patients with hypercalcemia of malignancy
    • Because of the lag in the onset of effect, bisphosphonates should be combined with faster-acting therapeutic modalities, such as aggressive volume replacement with normal saline infusion and possibly calcitonin injections.
    • calcitonin has a short-lived effect on hypercalcemia because of tachyphylaxis and therefore should only be used as an interim step.
    • Cinacalcet is a calcimimetic agent that occupies the calcium sensing receptor and lowers serum calcium levels in patients with primary and tertiary hyperparathyroidism associated with chronic kidney disease. It is not effective and not approved for use in malignancy-associated hypercalcemia.
    • Increased calcitriol production associated with activated macrophages (granulomatous diseases and lymphomas) can be diminished by using corticosteroids. However, prednisone does not lower PTHrP levels and therefore is not useful in humoral hypercalcemia of malignancy.
    Hypercalcemia with low PTH level
    • The 25-hydroxy vitamin D level is elevated in states of vitamin D intoxication,
    • 1,25-dihydroxy vitamin D level is increased in
    o sarcoidosis,
    o granulomatous disease, and
    o lymphoma.
    Malignancy-associated hypercalcemia
    • The first test should be PTH not PTHrP
    • PTH low
    • PTHrP high
    • Bisphosphonates inhibit osteoclastic bone resorption and are particularly effective in hypercalcemia of malignancy.
    • zoledronate, a long-acting intravenous nitrogen-containing bisphosphonate, induces rapid and long-lasting hypocalcemic response.
    • Alendronate has a mild hypocalcemic effect but is not potent enough to combat acute severe hypercalcemia.
    • Glucocorticoids have classically been used in hypercalcemic states associated with production of 1,25-dihydroxyvitamin D3, such as lymphoma or granulomatous disorders.
    Hypercalcemia with normal PTH level
    • In an asymptomatic patient with mild hypercalcemia and an inappropriately normal parathyroid hormone level the main differential includes primary hyperparathyroidism versus benign familial hypocalciuric hypercalcemia.
    • Familial hypocalciuric hypercalcemia is diagnosed by a urinary calcium/creatinine clearance ratio <0.01
    • In familial hypocalciuric hypercalcemia there is hypocalciuria while in primary hyperparathyroidism there is hypercalciuria

    Hungry bone syndrome
    • severe hypocalcemia and hypophosphatemia
    • can occur after removal of a parathyroid adenoma in patients with significant hyperparathyroid bone disease
    • The associated hypoparathyroidism is usually transient because the healthy parathyroid glands recover function quickly, generally within 1 week
    • Treatment with calcium and a short-acting vitamin D metabolite may be required until the bones heal.

    Hyperparathyroidism
    • Alkaline phosphatase levels are not elevated in all types of hyperparathyroidism
    • Although the action of PTH is to increase the renal tubular reabsorption of calcium, hypercalcemia causes an increase in the filtered load of calcium. This increase overwhelms the ability of PTH to reabsorb calcium in the renal tubule with resultant hypercalciuria

    Vitamin D deficiency,
    • characterized by
    o hypocalcemia,
    o hypophosphatemia,
    o increased alkaline phosphatase
    o increased parathyroid hormone levels,
    o decreased serum 25-hydroxy vitamin D level.
    • Measurement of 25-hydroxy vitamin D (calcidiol) is more informative than measurement of 1,25-dihydroxy vitamin D (calcitriol) in most patients with hypocalcemia because
    o vitamin D deficiency causes hypocalcemia and stimulates parathyroid hormone secretion, which in turn stimulates renal conversion of 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D. the 1,25-dihydroxy vitamin D level is influenced more by parathyroid hormone and phosphorus levels and by renal function.
    o Low dietary intake, poor absorption of vitamin D, and lack of production in the skin will result in a low serum 25-hydroxy vitamin D level.
    o This serum level will also be low in patients taking phenytoin, those with nephrotic syndrome (loss of vitamin D–binding protein), and those with hepatobiliary disease.
    o Whereas 25-hydroxy vitamin D has a long half-life, 1,25-dihydroxy vitamin D is more short-lived and therefore not a good measure of vitamin D status.
    o 1,25-Dihydroxy vitamin D levels will be low despite normal or high 25-hydroxy vitamin D levels in patients with
     renal insufficiency,
     deficiency of renal 1α-hydroxylase (vitamin D–dependent rickets type 1), or
     hypoparathyroidism.
    • The serum level of osteocalcin is not a specific marker of vitamin D deficiency and is not indicated. he level is elevated in disorders that increase the metabolic turnover of bone, such as Paget disease and osteomalacia.


    Secondary hyperparathyroidism due to vitamin D deficiency.
    • low vitamin D level,
    • low-normal serum calcium and phosphorus levels,
    • elevated parathyroid hormone level.
    • best treated with high-dose ergocalciferol therapy.
    • Calcitriol, or 1,25-dihydroxycholecalciferol, is a vitamin D3 analogue. It is most useful in patients with decreased synthesis of calcitriol, as occurs in hypoparathyroidism and chronic renal failure. Calcitriol therapy would not replete the body stores of vitamin D because it is given in very low doses because of its enhanced potency, compared with ergocalciferol, and so is inappropriate treatment for this patient.

    Vitamin D deficiency and primary hyperparathyroidism.
    • In uncomplicated "without Vit D deficiency" hyperparathyroidism cause hypercalciuria.
    • Vitamin D deficiency is common, especially in older patients, and can mask the severity of primary hyperparathyroidism. In such patients,
     the parathyroid hormone level is disproportionately elevated compared with the serum calcium level, and
     urine calcium excretion is often normal
    • The 25-hydroxyvitamin D level reflects total body stores of vitamin D and is thus the most appropriate to measure
    • If the serum calcium level and urine calcium excretion increase substantially with supplementation of vitamin D Then parathyroidectomy would then be necessary.

    Parathyroid cancer
    • is rare and the only feature that may make you suspicious of a cancer rather than adenoma is the grossly elevated PTH.
    Primary hyperparathyroidism management
    Parathyroidectomy for patients with asymptomatic primary hyperparathyroidism and any one of the following four criteria:
    1. Serum calcium concentration greater than 11.5mg/dL (2.85mmol/L)
    2. Creatinine clearance reduced to less than 60 mL/ min
    3. Bone mineral density T score less than −2.5 "osteoporosis" at any site or a previous fragility fracture
    4. Age younger than 50 years
    Hypoparathyroidism in alcoholism
    • Hypomagnesemia in the patient with alcoholism can mimic hypoparathyroidism, including severe hypocalcemia and hyperphosphatemia.
    • It causes both suppression of PTH secretion and resistance to PTH action
    • Measurement of PTH, vitamin D, and phosphate should be done if the magnesium level is normal in the setting of hypocalcemia.
    Pseudohypoparathyroidism
    • Tissue resistance to the action of PTH
    • increased PTH levels
    • hypocalcemia and
    • hyperphosphatemia.
    • Phenotypically, a short round face, short neck, and short fourth metacarpal bone. Obesity Dental hypoplasia Soft tissue calcification/ossification.
    • The diagnosis is confirmed with genetic analysis and with a failure of cyclic adenosine monophosphate (cAMP) rise following PTH.
    • Slipped femoral epiphysis is a recognised feature.
    •
    Pseudo-pseudohypoparathyroidism
    • phenotypic appearance of pseudohypoparathyroidism but normal calcium and phosphorus levels because of normal PTH secretion, function, and action.
    Familial hypocalciuric hypercalcemia
    • is a rare autosomal dominant disorder that is diagnosed by a urine calcium to creatinine clearance ratio of less than 0.01.
    • Clinical features
    • Most cases: Asymptomatic (unlike primary hyperparathyroidism)
    • Hypercalcaemia
    • Hypocalciuria ( Ca excretion rate < 0.02 mmol/L).
    • Normal to high PTH
    • Hypermagnesaemia
    • Green colored urine
    • Genetic testing for FHH-associated mutations in CASR
    • No treatment is generally required, as bone demineralisation and kidney stones are relatively uncommon in the condition
    Oncogenic osteomalacia
    • Occur in Certain tumours. prostatic carcinoma, and haematological malignancies such as myeloma and chronic lymphocytic leukaemia
    • produce a phosphaturic substance.
    • Clinically, patients present with bone pain and or fracture, profound proximal myopathy and severe hypophosphataemia, usually accompanied by a marked reduction in concentration of 1,25-OH vitamin D.
    • Other abnormalities of renal function such as glycosuria and aminoaciduria may also be present.
    • Treatment with vitamin D metabolites and phosphate supplements may result in some resolution of skeletal symptoms.
    • In the case of solid tumours, removal of the primary tumour also results in improvement of symptoms.


    Osteoporosis
    • Once yearly intravenous infusion of zoledronate is a potent therapy for treating postmenopausal osteoporosis

    Paget’s disease
    • Recent evidence has suggested that limited skeletal survey is superior to bone scan for the assessment of the disease.
    • Paget’s is present in around 2% of the population over 55 years, this prevalence increases with age and the disease is also more common in men
    • Deafness may be a feature in up to half of all patients with skull base Paget’s.
    • Osteogenic sarcoma is a very rare complication of the disease.
    • The mainstay of treatment is with bisphosphosphonates.
    • The goals of therapy in Paget’s disease are to normalise bone turnover and achieve an alkaline phosphatase as a marker of this, in the normal range if possible.
    • Bisphosphonates have become the mainstay of therapy,
    • It appears that the more aggressive initial therapy is, then the longer a period of remission may be achieved.
    • Alkaline phosphatase, as a non-invasive method, appears to be the best way to monitor disease activity.
    • Deafness may occur in up to half of patients with skull base Paget’s,
    • spinal cord compression may also occur.
    • Rarer complications include hydrocephalus and osteogenic sarcoma. Sarcomas are found most commonly in the humerus or femur and a rapid increase in pain in one limb may arouse suspicion, although it may of course just be a marker of increased disease activity.


    Medullary thyroid carcinoma
    • Important next investigation is Pentagastrin stimulation test NOT Random calcitonin
    • Elevated basal levels of calcitonin are seen in pregnancy, carcinoid, pernicious anaemia, chronic renal failure and thyroiditis.
    • The pentagastrin test measures calcitonin levels at 2 and 5 minutes however, and a rise in calcitonin is suggestive of medullary thyroid carcinoma.


    Cushing
    • Thin skin and loss of subcutaneous fat is a sign of Cushing's disease
    • Urinary free cortisol,,,, False positive results may be seen, particularly in obesity or if there is significant alcohol consumption
    • In patients with renal failure, Urinary free cortisol this test is more likely to give a false negative the most appropriate test in these circumstances would be an overnight dexamethasone suppression test
    • In patients with documented hypercortisolism,
    o elevated or normal ACTH levels indicate a pituitary or neoplastic (ectopic) source,
    o whereas suppressed ACTH concentrations indicate a primary adrenal source.
    • Partial suppression of ACTH achieved with high dexamethasone administration, suggests an ACTH-secreting pituitary microadenoma
    • MRI findings are normal in 40% to 50% of patients with documented ACTH-secreting pituitary adenomas.
    • Bilateral petrosal sinus catheterization should be performed in patients with biochemically established adrenocorticotropic hormone–dependent Cushing syndrome who have negative findings on pituitary MRIs and chest CT scans. the best way of distinguishing between ectopic and pituitary dependent CS is with inferior petrosal sinus sampling where a high gradient of ACTH from sinus compared with a peripheral sample is diagnostic of pituitary dependent disease.
    • Usually the cause of Cushing's disease is a pituitary microadenoma and this may not be seen on MR.
    • CT scan and octreotide scintigraphy should be employed when results of IPSS suggest an ectopic source.
    • The most appropriate next step is removal of the pituitary microadenoma by pituitary adenomectomy.
    • Bilateral adrenalectomy is an appropriate option in patients with ectopic ACTH secretion and an occult or metastatic tumor.
    • Ketoconazole can be used to lower cortisol secretion. However, this drug is used not as a definitive therapy for hypercortisolism but instead as an interim therapy for patients with severe Cushing syndrome.
    • Ketoconazole is also used in patients with recurrent or inoperable ACTH-secreting tumors and is often given as an interim therapy for patients undergoing radiation therapy because the beneficial effect of radiation treatment may be delayed.
    • Conventional radiation therapy leads to the normalization of urine free cortisol production in over 80% of patients, usually within 2 years. Radiation therapy is reserved for patients who cannot tolerate surgery or as a secondary treatment when pituitary surgery has failed
    • Secondary adrenal insufficiency due to exogenous corticosteroids may be associated with suppression of both ACTH and cortisol levels and with clinical findings of excess glucocorticoids.
    • Outcome analyses suggest that pregnant patients with newly diagnosed Cushing syndrome of all causes should undergo surgery, unless they are near term.
    • 2-day dexamethasone-corticotropin releasing hormone stimulation test would distinguish pseudo-Cushing's from autonomous glucocorticoid production
    • Hypogonadotropic hypogonadism with diminished libido and loss of secondary sexual characteristics

    Overnight dexamethasone suppression test
    • The overnight dexamethasone suppression test is usually used as a screening test for Cushing's syndrome.
    • This test has a false-positive rate of up to 2–12%,
    • Dexamethasone is primarily metabolised by the cytochrome P-450 system, by hepatic CYP3A4, an enzyme complex responsible for the metabolism of many xenobiotics.
    • Considerable increases in cytochrome P-450 enzymes can be seen in
    o regular smokers and people who
    o drink alcohol regularly.
    o Several drugs such as phenobarbital, primidone, ethosuximide, carbamazepine and rifampicin induce the activity of CYP3A4, and can lead to false positive dexamethasone suppression tests.

    Adrenal insufficiency during stress
    • Major stress give Stress-level dosages of corticosteroids are considered to be 10-times the normal daily replacement dosage. equivalent to 100 mg of hydrocortisone daily, best administered as 25 mg every 6 hours.
    • Minor stress (such as a common cold), doubling of the oral dosage of hydrocortisone for 2 days is recommended; for
    • Moderate stresses (such as a limited surgical procedure), tripling the dosage for 2 to 3 days is adequate.
    • Once the dosage of hydrocortisone is over 60 mg per day, fludrocortisone is unnecessary because that dose of hydrocortisone has adequate mineralocorticoid activity.
    Adrenal insufficiency with hypothyroidism
    • Thyroid hormone replacement can worsen symptoms or even precipitate an adrenal crisis in patients with underlying adrenal insufficiency. Due to increase the clearance of cortisol
    • Once adrenal insufficiency is confirmed, glucocorticoid replacement should be initiated before restarting or adjusting the levothyroxine therapy.
    Addison’s disease
    • Presentation
    o hyperkalemia,
    o hyponatraemia,
    o ureamia,
    o hypoglycaemia,
    o mild acidosis,
    o hypercalcaemia,
    o neutropenia,
    o lymphocytosis,
    o eosinophilia,
    o anaemia
    o abnormal liver function tests.
    o Low aldosterone secretion (leading to salt wasting)
    o High plasma renin
    o High adrenocorticotrophic hormone (ACTH)
    o High lipotropin
    o Elevated plasma vasopressin and Angiotensin II.
    o Primary hypoadrenalism may also cause mild hypercalcaemia and derangement of the thyroid function tests.
    • Causes
    o autoimmune destruction of the adrenal glands. Adrenal autoantibodies are present in about 75% of cases.
    o The next most common cause is TB.
    o Other causes include haemorrhage including
    • during pregnancy,
    • sepsis including Waterhouse–Friderichsen syndrome from meningococcaemia,
    • shock,
    • coagulopathy and
    • metastases.
     Other causes are
     metastases in over 90% in both glands,
     HIV and
     opportunistic infections associated with AIDS.

    Pheochromocytoma
    • Patients present with a variety of symptoms including
    o episodic hypertension,
    o chest tightness,
    o abdominal pain,
    o vomiting,
    o sweating,
    o restlessness, anxiety, pallor and
    o weakness.
    • Symptoms are precipitated by sneezing, stress, surgery and by agents such as cheese, alcohol and tricyclic antidepressants.
    • Glycosuria occurs during attacks in 30% of cases.
    • Tests that help in diagnosis include 24-hour catecholamine measurement, metaiodobenzylguanidine (MIBG) and CT/MRI of the adrenal glands.
    • it can also present with severe hypotension from catecholamine-induced cardiomyopathy
    • Approximately 10% of tumours are extra-adrenal (sometimes called paragangliomas), 10% are bilateral and 10% are malignant.
    • Phaeochromocytomas are associated with a number of syndromes including multiple endocrine neoplasia (MEN) 2A and MEN 2B.
    • Diagnosis is made by demonstrating elevated catecholamine levels in a 24-h urine sample.
    • A scan with 131iodine-labelled metaiodobenzylguanidine (MIBG) is used in cases where a tumour is confirmed biochemically but cannot be identified on computerized tomography (CT) or magnetic resonance imaging (MRI) scanning




    Liddle’s syndrome

    • hypokalaemic alkalosis
    • suppressed aldosterone
    • suppressed renin
    • hypertension.
    • an autosomal dominant
    • mutation in genes mapped to chromosome 16.
    • This leads to activation of sodium/potassium exchange independent of circulating mineralocorticoid.
    • Hypertension and hypokalaemia respond well to amiloride but not spironolactone, because amiloride acts directly on the sodium channel, whereas spironolactone acts on the mineralocorticoid receptor


    Renal artery stenosis
    • Hypertension
    • High renin
    • High Aldosterone
    • Secondary hyperaldosteronism








    Multiple endocrine neoplasia type 2
    • hyperparathyroidism due to parathyroid hyperplasia.
    • The most important is removal of pheochromocytoma. Then , a thyroidectomy and subtotal parathyroidectomy (removal of 3 ½ parathyroid glands) will be needed

    Amenorrhea
    • Pregnancy should be excluded in all patients prior to other evaluations.
    • Polycystic ovary syndrome is the most common cause of secondary amenorrhea
    • Laboratory evaluation is
     first directed toward ovarian failure,
     hyperprolactinemia, A high serum prolactin level requires additional pituitary evaluation, including MRI.
     thyroid disease.
    o An FSH greater than 20 mU/mL (20 U/L) suggests ovarian failure.
    • If the woman is younger than 30 years or has primary amenorrhea, obtaining a karyotype is often recommended, even if the stigmata of Turner syndrome are not present.
    • If the screening laboratory studies do not reveal a diagnosis, the cornerstone of further evaluation is a progestin withdrawal challenge with medroxyprogesterone acetate, 10 mg/d orally for 10 days, or micronized progesterone, 200 mg/d orally for 12 days.
    o Menstruation with progestin withdrawal indicates normal estrogen production and a patent outflow tract, which categorizes the amenorrhea as chronic anovulation with a normal estrogen level.
    o The absence of menses with progestin withdrawal indicates a low estrogen level and/or an anatomic defect. The pelvic anatomy, therefore, should be assessed with ultrasonography, MRI, or hysterosalpingography.
    Polycystic ovary syndrome
    • PCOS affects 6% of women of child-bearing age and typically presents with oligomenorrhea and signs of androgen excess (hirsutism, acne, and occasionally alopecia).
    • Polycystic ovary syndrome (PCOS) is the most common etiology of hirsutism with oligomenorrhea. This form of hirsutism normally starts at puberty or several years later and is slowly progressive. Furthermore, the serum testosterone level in women with PCOS rarely exceeds 150 ng/dL (5.2 nmol/L)
    • Insulin resistance is a major feature of the disorder, as are overweight and obesity, although only 50% of affected women are obese.
    • Typically, there is a
    o mild elevation in testosterone and dehydroepiandrosterone sulfate levels and a
    o luteinizing hormone to follicle-stimulating hormone ratio of greater than 2:1.
    o Normal oestradiol would be expected in PCOS
    o functional hyperprolactinaemia
    • Diagnosis requires two of the three following features:
    1. ovulatory dysfunction,
    2. laboratory or clinical evidence of hyperandrogenism,
    3. ultrasonographic evidence of polycystic ovaries.
    4. transvaginal ultrasound is said to have 91% diagnostic sensitivity for the condition in experienced hands. The presence of more than eight follicular cysts of less than 10 mm and increased ovarian stroma is sufficient to make the diagnosis.
    • Normal 17-hydroxyprogesterone level excludes nonclassic 21-hydroxylase deficiency as a diagnosis. Therefore, corticosteroid (prednisone) therapy is not indicated.
    • Weight loss is the gold-standard treatment for PCOS, and improves ovulation, androgen levels, hirsuitism and metabolic features associated with insulin resistance.
    • A loss in weight of only 5% reduces hirsuitism by up to 40%.
    • In patients with hirsutism and polycystic ovary syndrome who do not wish to become pregnant, the most appropriate initial therapy after weight loss is oral contraceptive pill Then spironolactone
    Non-classical congenital adrenal hyperplasia
    • hirsutism.
    • hypogonadotrophic hypogonadism,
    • low oestradiol
    • normal concentrations of luteinising hormone (LH) and follicle-stimulating hormone (FSH)
    • a slightly raised testosterone concentration and
    • 17-OHP concentration above 33 nmol/l would be diagnostic.
    Cushing's syndrome and Amenorrhea
    • hirsutism.
    • hypogonadotrophic hypogonadism,
    • low oestradiol
    • normal concentrations of luteinising hormone (LH) and follicle-stimulating hormone (FSH)
    • a slightly raised testosterone concentration
    • free cortisol could provide useful information.
    Pregnancy and Amenorrhea
    • Very high oestradiol
    • High prolactin
    • suppressed luteinising hormone/follicle-stimulating hormone (LH/FSH)




    Amenorrhea And adrenal or ovarian tumor
    • Rapid virilization rapidly developed progressive hirsutism, acne, and a deepened voice
    • very high testosterone level. Such a high level (>200 ng/dL [6.9 nmol/L]) need abdominal and pelvic CT scan.
    Functional hypothalamic amenorrhea,
    • which is usually caused by excessive loss of body weight or fat or excessive exercise as in anorexia nervosa, is a diagnosis of exclusion includes
    o a pregnancy test and
    o measurement of serum prolactin,
    o thyroid-stimulating hormone, and
    o follicle-stimulating hormone
    • BMI is typically less than 17.
    • If a functional etiology is still suspected, decreased exercise, improved nutrition, and attention to emotional needs are helpful adjuncts to restore normal menses and fertility.
    • Low estradiol with normal or low LH FSH
    Overweight amenorrhea in young women
    • Pregnancy
    • PCOS need US of pelvis
    • Cushing syndrome
    • hypothyroidism and
    • hypothalamic disease. there is often a prior history of trauma (or neoplasia) to the brain. As a result patients can develop excessive appetites.
    Hirsutism
    • New-onset hirsutism with virilization, particularly in an older woman, and accompanied by a serum total testosterone level >200 ng/dL (6.9 nmol/L) is almost always due to a tumor.


    Prostate and Hypogonadism
    • Men with hypogonadism often have a low prostate-specific antigen level that doubles with therapy and then stabilizes by 6 months after therapy initiation; a greater increase should indicate discontinuation of therapy and evaluation for prostate cancer.
    Kallmann syndrome
    • hypogonadotrophic hypogonadism
    • absent sense of smell.
    • Absent olfactory bulbs are present on 75% of MRI scans in these patients.
    • The syndrome results in absence of GNRH.
    • This patient should be managed with androgen replacement therapy
    • fertility can be restored in the majority of patients with either pulsed GNRH or gonadotrophin therapy.
    • Once fertility treatment stops " who do not desire fertility " it is necessary to give testosterone for men and oestrogen and progestins for women
    • The main health risk, for both men and women, of untreated Kallmann Syndrome is osteoporosis. Therefore, regular bone-density scans (every two years ) are advisable
    Acquired hypogonadotrophic hypogonadism
    • Low testosterone and gonadotropin levels
    • Sleep apnea has been associated with hypogonadism and can be reversed by application of continuous positive-airway pressure… testosterone replacement therapy can worsen sleep apnea, so do sleep study first.
    • Common causes
    o pituitary tumors,,,prolactinoma,,,, Hyperprolactinaemia may be associated with a HH and signs such as galactorrhoea may be present. pituitary MRI would be the best imaging technique
    o trauma
    o infiltrative diseases (such as hemochromatosis).
    o chronic illnesses,
    o malnutrition,
    o obesity, and aging.
    o drugs include alcohol, Anabolic corticosteroids, opioid-induced hypogonadism cocaine, and ketoconazole.
    Hypogonadism and Testosterone level
    • patient, who is normal weight, with normal total testosterone level, it is very likely that his free testosterone level will also be normal
    • A discrepancy in the levels can occur in obese men in whom the sex hormone–binding globulin (SHBG) level is decreased, which causes a decrease in the total testosterone level.
    • SHBG may increase with age, so that measurement of free testosterone levels may be helpful when assessing gonadal function in older patients.
    Hypogonadism
    • The best screening test for male hypogonadism is an early morning measurement of the total testosterone level.
    • A random serum testosterone level greater than 350 ng/dL (12.15 nmol/L) excludes hypogonadism. Values consistently less than 200 ng/dL (6.94 nmol/L) almost always confirm hypogonadism, but values in the 200 to 350 ng/dL (6.94-12.15 nmol/L) range are equivocal.
    • If the level is equivocal, a second measurement, which includes free and bioavailable testosterone levels and/or the SHBG level,
    • PRL, LH, and FSH levels also are measured to determine the type of hypogonadal state and to guide further evaluation and treatment.


    Hypergonadotrophic hypogonadism
    • High LH,FSH
    • Low testosterone
    • Causes
    o Klinifelter,,,, need Karyotype study "primary infertility" NO children
    o Testicular tumour, infiltration or idiopathic failure secondary infertility patient may have children ultrasonic evaluation of the testes is the most appropriate investigation

    Type 1 polyglandular syndrome
    • mucocutaneous candidiasis,
    • hypoparathyroidism and
    • Addisons, whereas
    Type 2 polyglandular syndrome
    • addisons,
    • hypothyroidism and
    • Type 1 diabetes,
    • hypogonadism,
    • coeliac and
    • myasthenia gravis may also be seen.

    Adrenal Incidentaloma
    • Clinically inapparent adrenal masses are discovered in 0.4% to 6.9% of imaging studies performed during evaluation of nonadrenal disorders.
    • Most adrenal nodules are hormonally silent and have no malignant potential. As many as 30%, however, secrete cortisol, aldosterone, androgens, or catecholamines.
    • In patients with normal BP who have an incidentally discovered adrenal nodule,
    o Subclinical Cushing syndrome should first be excluded with an overnight 1-mg dexamethasone suppression test.
    o A screening test for pheochromocytoma (by measurement of the plasma metanephrine level) is also recommended by most experts, even if the patient is normotensive. The rationale for screening is that patients with pheochromocytoma may only be intermittently hypertensive.
    • In patients with hypertension who have an incidentally discovered adrenal nodule,
    o screening for hypercortisolism and
    o pheochromocytoma is essential, as is
    o measurement of serum aldosterone and plasma renin activity.
    • Adrenal androgens, such as dehydroepiandrosterone sulfate, should only be assessed in masculinized female patients, just as the estrogen level should be measured in feminized male patients.

    Osteoporosis
    • Progressive osteoporosis in a patient on bisphosphonate therapy who has adequate calcium and vitamin D intake is an indication to change the bisphosphonate to teriparatide. (recombinant human parathyroid hormone) is given via daily subcutaneous injection for a recommended duration of 1 to 2 years. Teriparatide can significantly decrease the incidence of both vertebral and nonvertebral fractures.
    • Because animal studies have shown an increased risk of osteosarcoma, this agent should be avoided in patients with
    o Paget disease of bone,
    o previous radiation therapy involving the skeleton, or
    o a history of skeletal cancer.
    polyuria and polydipsia
    • Causes
    o diabetes mellitus (prevalence 4%),
    o hypercalcaemia (prevalence 1–4%) and
    o hypokalaemia.
    o Diabetes insipidus is rare (prevalence: 1 in 25,000).
    • Initial laboratory screening for polyuria and polydipsia
    o U+E,
    o calcium, and
    o glucose.
    o If these tests are normal, investigations should be directed towards rarer causes.
    Hyponatraemia
    Hypervolaemic hyponatraemia,
    • elevated JVP,
    • ascites, and
    • peripheral oedema,
    • caused by renal, cardiac, or liver failure.
    Hypovolaemic hyponatraemia
    • caused by salt loss, usually from the kidneys or gut.
    • tachycardia, hypotension, dry mucous membranes
    • low JVP.
    • Laboratory features include elevated serum urea and sometimes creatinine.
    • The source of salt loss (gut or kidney) can be identified with a urinary sodium;
    o a value greater than 20 mmol/l indicates renal loss.
    Euvolaemic hyponatraemia
    • cause primarily by SIADH and hypothyroidism.
    • Serum urea is normal or low.
    Anorexia nervosa
    • normocytic normochromic anaemia due to bone marrow suppression,
    • hypokalaemia from laxative abuse,
    • metabolic alkalosis resulting from vomiting and the gastrointestinal loss of HCl,
    • hypocalcaemia from dietary deficiency and the associated protein deficiency, and
    • increased serum amylase level from frequent vomiting.
    Gitelman’s syndrome
    • hypokalaemic alkalosis
    • NO hypovolaemia
    • NO hypertension.
    • presenting at older age
    • caused by mutation in the thiazide-sensitive Na-Cl transporter
    • resultant salt wasting leads to activation of the renin-angiotensin system also leading to raised aldosterone levels
    • Gitelman’s is associated with hypocalciuria and
    • hypomagnesaemia.
    • Treatment is with potassium and magnesium replacement.
    • Where patients fail to respond to supplementation, potassium sparing diuretics may be required to restore serum potassium levels.
    Thiazide abuse
    • normal BP,
    • hypokalaemia and
    • high bicarbonate
    Bartter's syndrome
    • usually presents in childhood with polyuria,
    • nocturnal enuresis and
    • growth retardation
    Obesity
    • An anti-obesity drug should only be considered for those with a body mass index (BMI) of 30 kg/m2 or greater in whom at least three months of managed care involving supervised diet, exercise and behaviour modification fails.
    • If risk factors (for example, diabetes mellitus, coronary heart disease, hypertension and obstructive sleep apnoea) are present, it may be appropriate to prescribe a drug to individuals with a BMI of 28 kg/m2 or greater.
    • Anti-obesity drug treatment should also be discontinued if weight loss is less than five percent after the first 12 weeks.
    • Combination drug therapy is contraindicated at present and drugs should never be used as the sole element of treatment.
    • Diet and exercise have been shown to be ineffective over the long term.

    Mixed metabolic and respiratory alkalosis
    pH 7.66 (7.36-7.44)
    pO2 7.4 kPa (11.3-12.6)
    pCO2 4.6 kPa (4.7-6.0)
    HCO3 34 mmol/L (20-28)


    Features of laxative abuse include:
    • Hypokalaemia
    • Metabolic alkalosis
    • Clubbing
    • Diarrhoea whilst nil by mouth
    • Loss of haustral pattern on barium enema but relatively normal macroscopic appearance
    • Pigmentation of colonic mucosa (anthracenes, e.g. senna) and sometimes skin
    • Pseudostrictures from spasm lasting hours
    • Raised stool magnesium (osmotic laxatives)
    • Uric acid kidney stones
    • Osteomalacia
    • Protein-losing enteropathy

    Somatostatinomas are exceedingly rare, and are characterized by the triad of
    • cholelithiasis,
    • steatorrhoea and
    • diabetes.
  35. Dr Hopeful

    Dr Hopeful Guest

    Dr Albarwari ....there is always one FUNNY guy. I would not worry about empty / shallow threats
  36. failed  doc

    failed doc Guest

    thank you brawrri you are good man
  37. guest430

    guest430 Guest

    yes dr albarwari

    don take risks if u r getting such mails

    ow every body can make their own notes, i think they got an idea
  38. OKO

    OKO Guest

    Dr Albarwari Can you send me the notes at mail

    FindingHimo@Gmail

    Continue to publish Man , Go On
  39. RNA

    RNA Guest

    GREAT.....KEEP THE GOOD WORK FLOWING....MAY ALLAH SUCCEED U
  40. dodo.

    dodo. Guest

    from these note for all who sit the exam now and previous can anyone tell us what single choice he could answerd in his previous attempt from such notes ...its from pastest..
  41. score

    score Guest

    @dr. jim.....

    doc, where are u based in india?
  42. Dr albarwari

    Dr albarwari Guest

    GIT and Hepatology


    Achalasia
    • It can present at any age with
    o intermittent dysphagia to both solids and liquids,
    o regurgitation,
    o severe retrosternal chest pain and
    o aspiration pneumonia.
    • A chest X-ray may show an air-fluid level behind the heart.
    • Barium swallow usually shows dilatation of the oesophagus with a tapering lower end, and the loss of normal peristalsis.
    • Upper gastrointestinal endoscopy should always be performed in suspected achalasia to exclude a tumour, which can present similarly
    • However, all these investigations may be normal and
    • The definitive diagnostic test is oesophageal manometry
    • Treatment options include
    o endoscopic pneumatic dilation of the LOS (successful in 80% of cases),
    o intra-sphincteric botulinum toxin injection or
    o surgical division of the LOS (Heller’s cardiomyotomy).
    • A 7% increase in squamous cell carcinoma over 25 years
    Oesophageal diseases and manometry
    • Scleroderma cause low resting lower oesophageal sphincter (LOS) pressure
    • Gastro-oesophageal reflux disease
    o cause low LOS pressure
    • Nutcracker oesophagus,
    • Non-specific oesophageal dysmotility,,,
    o failure of LOS relaxation (high residual pressure)
    • Oesophageal spasm
    o failure of LOS relaxation (high residual pressure)
    • Achalasia
    o absent distal peristalsis which may be accompanied by a high resting LOS pressure.
    • Candida causes
    o odynophagia (painful swallowing) rather than dysphagia, and is not associated with any specific manometric findings.
    • Globus is a psychological condition and should only be diagnosed in the absence of abnormal findings
    • Extrinsic compression form hilar tumours can be missed on endoscopy but do not result in recognised patterns at manometry.
    Nutcracker esophagus
    • is a disorder of the movement of the esophagus
    • dysphagia, to both solid and liquid foods,
    • chest pain
    • may also be asymptomatic.
    • Age : 6th and 7th decades of life.
    • Diagnosis is made by an esophageal motility study
    o "increased pressures during peristalsis" with a diagnosis made when pressures exceed 180 mmHg;
    o LOS relaxes normally in nutcracker esophagus, but has an elevated pressure of greater than 40 mm Hg at baseline
    • Medical therapy
    o calcium-channel blockers
    o isosorbide dinitrate
    o sildenafil
    o botulinum toxin

    Oesophageal carcinoma
    • The diagnostic test of choice remains histology.
    • Once diagnosis is confirmed, a CT scan is necessary to stage disease for disease extent and to consider surgical resectability.
    • The incidence of adenocarcinoma in the UK is rising, while that of squamous-cell carcinoma is falling.
    • If the patient has metastases as demonstrated by the presence of enlarged supraclavicular nodes, and therefore would not be a suitable candidate for oesophagectomy
    • Squamous cell carcinoma of the oesophagus is more responsive to radiotherapy than adenocarcinoma
    • 5-year survival after radiation therapy is put at between 6% and 20%.
    • Oesophageal stents are used in the treatment of tracheo-oesophageal fistulas and palliation in advanced disease.
    • Presently, there are no genetic screening tests for oesophageal carcinoma.
    Oesophageal perforation
    • History of Severe gastroenteritis is associated with vomiting and diarrhoea.
    • Sudden-onset chest pain
    • pleural effusion
    • A gastrograffin swallow, will demonstrate the site of the perforation.

    Barretts esophagus Recommendation
    • Low grade
    o 8-12 weeks of continuous high dose PPI and then
    o re-endoscopy ,,,,If some improvement is seen then
    o 6 monthly review is suggested until stable / improved disease has been identified on at least 2 successive endoscopies. Once this milestone has occurred then
    o surveillance can be reduced to 2 yearly.
    • High grade
    o associated with a focus of invasive adenocarcinoma in 30–40% of patients.
    o if the changes persist after intensive acid suppression high dose PPI and are confirmed by two expert pathologists, then
    o oesophagectomy is currently recommended But
    o In those unfit for surgery, endoscopic ablation or mucosal resection should be considered

    NICE Guideline for high grade
    o Consider offering endoscopic therapy as an alternative to oesophagectomy to people with high-grade dysplasia and intramucosal cancer , taking into account individual patient preferences and general health.
    o Endoscopic therapy is particularly suitable for patients who are considered unsuitable for surgery or who do not wish to undergo oesophagectomy
    o Do not use in combination with each other argon plasma coagulation, laser ablation or multipolar electrocoagulation alone, or in combination with each other, unless as part of a clinical trial
    o If using endoscopic mucosal resection, consider following with an additional ablative therapy (radiofrequency ablation, argon plasma coagulation or photodynamic therapy) to completely remove residual flat dysplasia

    After Helicobacter eradication
    • is associated with a reduction in the risk of gastric maltoma and gastric carcinoma "so the patient can be reassured that she no longer has a significantly increased risk of GI cancer"
    • there is no specific need for re-dosing of eradication therapy,
    • oesophageal carcinoma is not related to Helicobacter

    Dyspepsia, in the absence of alarm symptoms
    • should be treated with
    o lifestyle advice and
    o PPI if needed 4 months
    • If after one month symptoms are not controlled then testing for Helicobacter pylori (breath test or serology) could be carried out.
    • There needs to be a two-week wash-out period off the PPI for hydrogen breath test to be reliable.
    Malabsorption + Low B12
    • Terminal ileal disease
    o Crohn’s disease," bimodal presentation with peaks between 15-30 years and between 60-80 years"
    o terminal ileal resection,
    o ileal tuberculosis,,, high ESR abnormal CXR
    o pernicious anaemia,,, but Symptoms of malabsorption are absent
    • Excess B12 utilisation in the gut by bacteria,,, Vitamin B12 is selectively metabolised by the bacteria and the folate is left so there is high folate + low B12
    o Small intestinal diverticulae, age 60-70 years
    o fistulae,
    o radiation enteritis " fibrotic strictures and adhesions" may occur after 5 years
    o systemic sclerosis
    • A normal serum gastrin excludes pernicious anaemia
    Celiac disease
    • faecal occult blood may be positive
    • secondary hyperparathyroidism may occur due to vitamin D deficiency
    • The best initial screening tests are serological either tissue transglutaminase or anti-endomysial antibodies, but
    • These tests may be invalid in the presence of selective IgA deficiency
    • Small bowel follow-through may show total or subtotal villous atrophy
    Short bowel syndrome
    • removal of more than one-half of the small intestine, malabsorption syndrome may result.
    • It may occur in patients with
    o Crohn’s disease or those with
    o ischaemic bowel who have undergone significant bowel resection.
    • Presentation with
    o diarrhoea and steatorrhoea,
    o weight loss,
    o anaemia,
    o osteoporosis/osteomalacia,
    o electrolyte disturbances and hypovolaemia
    o Renal and gall bladder stone "ileal resection"
    • Treatment
    o In patients with more than 100 cm of jejunum,
     oral intake
     lactose exclusion
     a course of metronidazole to eradicate bacterial overgrowth.
    o In patients with less than 100 cm of jejunum, total parenteral nutrition is recommended


    Colonic diverticulae and anemia
    • Presentation
    o cramping abdominal pains with
    o intermittent diarrhoea alternating with constipation
    o weight is steady
    • Lower GI blood loss may occur as frank haemorrhage or occult losses
    • Occult blood in the stool is present in approximately 25% of patients with diverticulitis.
    • Iron deficiency is therefore a commoner overall cause of anaemia related to this condition than is Vitamin B12 deficiency.
    • Vitamin B12 deficiency related to bacterial overgrowth and malabsorption is relatively uncommon in this condition
    Radiation enteritis
    • occurs 9 to 14 months following radiation exposure
    • Presentation
    o intermittent rectal bleeding,
    o loose stool
    o weight loss
    o obstructed defecation,
    o rectal pain or urgency.
    • results in a chronically ischaemic intestinal segment that may lead to stricture
    • Diagnosis can be
    o Barium enema shows luminal narrowing with some irregularity of the bowel wall
    o confirmed with colonoscopy
    o Biopsy is not diagnostic but is helpful to exclude other causes
    • Treatment
    o rectal sucralfate, metronidazole combined with topical anti-inflammatory treatment, and heater probe appear promising

    Inflammatory bowel disease
    • Indeterminate colitis
    o In around 10% of patients, it is impossible to distinguish ulcerative from Crohn’s colitis
    o ulcerative colitis is strongly associated with pANCA
    o the presence of anti-Saccharomyces cerevisiae antibodies favour Crohn’s disease.
    The criteria to determine ulcerative colitis severity include:
    1. Stool frequency >6
    2. ESR greater than 30 mm/hr
    3. pulse rate (greater than 90 bpm);
    4. temperature (greater than 37.8oC in 2 out of 4 days);
    5. anaemia (Hb <75% predicted). < 10.5g
    • In severe ulcerative colitis, patients should be treated with
    o intravenous Hydrocortisone "not oral prednisolone"
    o Rectal hydrocortisone also can be given
    o fluids,
    o potassium supplementation
    o subcutaneous heparin and
    o elemental diet.
    o No Antibiotics
    o The patient should also have daily examination and monitoring including
    • review by surgeons,
    • blood tests,
    • stool chart,
    • heart rate,
    • temperature and
    • abdominal X-rays.

    Woman with well-controlled crohn disease on azatioprine want to be pregnant
    • Stop azathioprine although there is no increase in fetal anomalies
     if her disease flares up again then azathioprine could be re-instituted
    • Give folic acid supplements
    • Give Low dose corticosteroids <20 mg instead of azathioprine
    o Give Stress doses of steroids should be used during labour and delivery if the mother received steroids (even low-dose) for more than 2-3 weeks
    o use of oral calcium and vitamin D supplements is recommended.
    o neonate should be monitored for evidence of adrenal insufficiency and infection


    Pregnant with exacerbated crohn disease presents with bloody diarrhea with tender PR
    • Flexible sigmoidoscopy is the most appropriate investigations
    • presence of bloody diarrhoea fits best with predominantly distal disease.
    • The bowel preparation is much more severe with colonoscopy than that for flexible sigmoidoscopy, and the procedure itself causes significantly more discomfort.
    • If distal disease is identified then rectal corticosteroids would be the treatment of choice.



    Cancer Screening in patient with ulcerative colitis
    • Patients with extensive UC should be screened 8 to10 years from the onset of symptoms by Colonoscopy
    • Second decade Colonoscopy should be performed 3-yearly
    • Third decade Colonoscopy should be performed 2-yearly
    • Fourth decade Colonoscopy should be performed yearly
    • Patients with concomitant UC and PSC Colonoscopy should be performed yearly
    • Patients post-liver transplant for PSC still should have yearly screening.
    Toxic megacolon
    • a severe colitis (almost always pancolitis)
    • dilatation of the colon >5.5 cm radiologically.
    • Causes
    o most often occurs in the context of ulcerative colitis,
    o but can also occur in Crohn’s,
    o pseudomembranous colitis,
    o ischaemic colitis and other
    o colitides.
    • It is an absolute contraindication to barium enema examination because of the risk of bowel perforation.
    • Mortality is high (around 20%),
    • Management
    o High-dose steroids and iv fluids
    o intravenous antibiotics
    o avoiding antidiarrhoeal drugs and opioid analgesics
    o knee-elbow position to aid evacuation of gas per rectum, and inserting a nasogastric tube to aspirate bowel gas and fluids
    o If no improvement is seen in 24 h, early surgery (usually colectomy) is indicated.




    Maintaining remission in Crohn’s disease
    • Thiopurines (azathiaprine and 6-mercaptopurine) are the most effective agents
    • If not tolerated, methotrexate could be used as an alternative.
    • 5-ASA compounds such as balsalazide and sulphasalazine have a role in maintaining remission and are generally well tolerated but are not as effective as thiopurines.
    • There is no role for steroids in maintaining remission – only in the treatment of acute flares as is the case with dietary modification.
    • Ciclosporin is only of value in acute severe ulcerative colitis.
    • Infliximab is of value in long-term remission in fistulating Crohn’s (and possibly in non-fistulating disease) but is generally use ed alongside a thiopurine).
    Differentiation between ulcerative colitis and whippl disease
    • Both have
     Sacroiliatis, Large joint arthritis
     Weight loss
    • But whippl has malabsorption "which is absent in ulcrative colitis as
     High MCV "B12 and folate deficiency"
    Intermittent melaena "Between episodes of melaena he is asymptomatic" Investigation
    • upper endoscopy and colonoscopy Then
    • In the stable outpatient setting, a Meckels scan may be more useful in excluding a Meckel diverticulum.
    • In centres where it is offered, capsule endoscopy may be a reasonable alternative to Meckel's scan.
    • A mesenteric angiogram is most effective during active blood loss not when the patient is asymptomatic
    • A barium swallow and barium enema will not find any part of the bowel not already seen by OGD and colonoscopy.

    Colovesical fistula
    • Recurrent urinary tract infections,
    • altered bowel habit,
    • brown discoloration of urine and
    • intermittent air bubbles on passing urine.
    • Causes of gastrointestinal fistulae include
    o crohns disease,
    o diverticulitis and
    o colorectal tumours

    Mesenteric ischaemia
    • Plain X-ray is often normal, although mucosal oedema and thumb printing
    • Mesenteric angiography is the best diagnostic test.
    • CT scan show evidence of bowel wall thickening and thumb-printing.
    • More than two thirds of patients with ischaemic colitis respond favourably and rapidly to simple conservative measures with spontaneous recovery within 24 to 48 h.
    • The remaining one-third requires exploratory laparotomy
    • Conservative management includes
    o close monitoring,
    o appropriate intravenous rehydration and
    o broad-spectrum antibiotics that cover enteric flora and
    o aggressive measures to correct processes that may have precipitated the ischaemic insult.
    • For those who do not settle or develop peritonism, surgery is required.
    Causes of bacterial bloody GE in the UK
    • campylobacter infection is the commonest cause
    • followed, by salmonella and shigella.

    Campylobacter GE
    • Infection usually arises from eating undercooked frozen food eg barbeques
    • colicky abdominal pain,
    • vomiting
    • blood mixed with diarrhoea.
    • pyrexial and clinically dehydrated
    • The symptoms are usually self-limiting, lasting up to 5 days

    Chronic pancreatitis
    • Diarrhea with bulky pale stools
    • Serum folate low
    • B12 low
    • Faecal elastase low
    • Causes
    o Alcohol (60-90%)
    o cystic fibrosis
    o Hypertriglyceridaemia,
    o autoimmune pancreatitis (e.g. associated with primary sclerosing cholangitis)
    o surgery
    o Hereditary pancreatitis (autosomal dominant)
    o pancreas divisum (congenital pancreatic abnormality of fusion),
    o hyperparathyroidism,
    o uraemia are rare causes.
    o Gallstones (more commonly associated with recurrent acute pancreatitis) may be a contributing cause in ~20-25% of cases.
    • Faecal elastase is a sensitive marker of pancreatic insufficiency
    • Imaging of the pancreatic duct and biliary tree by ERCP/MRCP Magnetic Resonance would however be required to exclude a mass lesion particularly in light of the significant weight loss.
    • In early disease there may be
    o no X-ray calcification of the pancreas
    o ERCP can be normal
    o CT Abdomen can also be normal

    Secretin test
    • chronic pancreatitis
    o normal volume (> 2 ml/kg) and
    o low in HCO3 (< 80 mEq/l)
    • pancreatic duct obstruction
    o low volume (< 2 ml/kg),
    o normal HCO3 (> 80 mEq/l)
    o normal enzyme levels suggest perhaps secondary to a tumour and should prompt ERCP.


    Pancreatic pseudocysts
    • They cannot be diagnosed until more than 6 weeks after the acute attack,
    • Presentation
    o abdominal pain
    o mass,
    o fever
    o persistently raised amylase and liver function tests.
    • Treatment
    o Small pseudocysts usually resolve on their own but
    o those that are greater than 6 cm in diameter seldom disappear spontaneously and may lead to complications such as haemorrhage and infection,,,managed by
     endoscopic or percutanous drainage or
     surgical intervention
    Acute mesenteric ischaemia
    • Risk factors of atherosclerosis
    o IHD recent history of myocardial infarction
    o diabetic,
    o smoker
    • Presentation
    o acute abdominal pain 15-30 min post-meal, Increased intestinal motility after a meal exacerbates ischaemia, causing pain
    o relative hypotension
    o acidosis
    • Investigations
    o modest elevations in amylase.
    o An arterial blood gas will no doubt show a metabolic acidosis
    o CT scan will help exclude
     necrosis of the pancreas,
    o mesenteric angiography
    • Treatment
    o laparotomy

    Meckel's diverticulum
    • males.
    • asymptomatic;
    • complications
    o haemorrhage,
    o volvulus and
    o intussusception, mostly in children younger than 10 years of age.
    • Diagnosis
    o Tc-99m pertechnetate scintigraphy In virtually all patients who present with bleeding, ectopic gastric mucosa can be demonstrated
    o Tc-99m has an overall specificity and sensitivity of 90% for establishing the diagnosis.
    • Once bleeding occurs, surgery is recommended.



    Multiple hamartomatous polyps in GIT tract
    • familial juvenile polyposis,
    • Cowden’s syndrome,
    • Peutz-Jeghers syndrome,
    • neurofibromatosis type one, and
    • Multiple endocrine neoplasia syndrome type 2, all
    • These syndromes are distinct from the more common adenomatous syndromes such as HNPCC and FAP

    Cowden’s syndrome
    • is an inherited
    • defect in the PTEN tumour suppressor gene.
    • oral mucosal papillomas,
    • palmoplantar keratoses and
    • trichilemmomas (benign tumours of hair follicles).
    • The syndrome is important to diagnose early because of the high risk of malignancy, particularly of the breast and thyroid.
    • Thyroid dysfunction is common even in the absence of cancer.

    Hereditary non-polyposis colorectal cancer syndrome
    • It is an autosomal dominant syndrome
    • early-onset colorectal cancer.
    • It may account for 1-2% of all cases of colorectal cancer
    (CRC).
    • In 55-60% of cases, cancers are right sided also at increased risk of cancer of the endometrium, stomach, small bowel and genitourinary tract.
    • Mutations responsible : DNA mismatch repair gene
    • HNPCC-related cancers in three or more relatives, one of whom is a first-degree relative of the other two
    • Individual at risk should be offered colonoscopic screening at 2-year intervals from the age 20-25 years which should be continued up to the age of 40 years
    Peutz–Jegher’s syndrome
    • an autosomal dominant
    • multiple hamartomatous polyps throughout the gastrointestinal tract " upper and lower GIT"
    • and mucocutaneous melanocytic macules.
    • The condition has equal sex
    • Germline mutation of the serine threonine kinase STK 11 gene on chromosome 19
    • There is significant risk of eventual malignant transformation
    • Almost 50% of all Peutz–Jegher patients develop and die from cancer by the age of 57 years.
    • The mean age at first diagnosis of cancer is 43 years.
    • The cumulative risks of cancer development are highest for the stomach, colon, pancreas and breast.
    • Regular surveillance examinations, endoscopies and ultrasound imaging (yearly) are recommended.
    •

    Zollinger–Ellison syndrome
    • The best initial screen is a fasting gastrin level on three separate days, as the secretion of gastrin is pulsatile.
    o Three samples in the normal range make a gastrinoma unlikely.
    • This is usually followed by basal acid output estimation and a secretin stimulation test.
    • After this, patients usually move on to imaging studies
    • Treatment
    o Surgical resection If there is no hepatic metastases
    o Intravenous and then oral proton pump inhibitors are useful in the acute situation to reduce acid secretion.
    o Octreotide, interferon and chemotherapy may be useful in non-surgically resectable lesions.
    Portal hypertension
    • Normal hepatic venous pressure gradient = Hepatic wedge pressure - Inferior vena cava pressure (normal HVPG = 1-5 mmHg)
    • If HVPG >5 mmHg it is PH
    • If HVPG >10 mmHg it is Clinical PH
    • Type of PH
    o If HVPG >5 mmHg it is either sinusoidal "intrahepatic" OR post-sinusoidal 'hepatic vein"
    o If HVPG <5 mmHg it is presinusoidal "portal vein" eg
    • Longstanding portal vein thrombosis
    • Schistosomiasis
    • Sarcoidosis




    Hepatorenal syndrome
    • Treatment,,,, drug which given intravenously to improve renal function is agonists of vasopressin V1 receptors such as terlipressin. This causes splanchnic vascoconstriction, which may reverse the early splanchnic vasodilatation seen in hepatorenal syndrome.


    Alcoholic hepatitis
    • pyrexial
    • leucocytosis,
    • Hepatic decompensation with coagulopathy,
    • encephalopathy and
    • ascites
    • The AST/ALT ratio is usually greater than 2
    • Ferritin is a non-specific acute phase reactant and is normally elevated in alcoholic liver disease
    Alcoholic fatty liver
    • The histological changes seen in the liver can return to normal within 2–4 weeks
    • develops more quickly in the female sex " business woman"
    • Liver function tests are deranged with an
    o increase in the aminotransferase levels
    o Gamma glutamyl transpeptidase (GGT) may be elevated in relation to alcohol use, it is neither specific nor sensitive.
    • Abstinence and an adequate diet are the mainstays of treatment
    • Excess alcohol use is a cause of a secondary hyperlipidaemia
    Non-alcoholic steatohepatitis
    • Whilst only approximately 2% of patients with fatty infiltration progress to cirrhosis and liver failure, where
    • Non-alcoholic steatohepatitis exists progression to cirrhosis is as high as 10%.
    • There is no proven treatment for NASH, but patients should be advised to lose weight.
    Chronic hepatitis B in pregnancy
    • Infants born to mothers known to carry hepatitis B can be treated with antibodies to the hepatitis B virus (HBIg). When given with the vaccine within twelve hours of birth, the risk of acquiring hepatitis B is reduced 90%.This treatment allows a mother to safely breastfeed her child
    Chronic hepatitis B
    • Chronic hepatitis B is defined as the persistence HBsAg in the circulation for more than six months after clinical infection.
    • HBeAg is a marker of infectivity
    • but patients with Hepatitis B virus (HBV) pre-core mutant
    o do not synthesise HbeAg ,,,
    o Typically patients have lower concentration of HBV DNA,,,,
    o Response to interferon is not good and relapse rates tend to be high.
    • Treatment of chronic hepatitis is aimed at patient with active disease and viral replication, preferably at a stage before cirrhosis has developed
    • The indication for hepatitis B treatment is based on
    1. abnormal alanine aminotransferase on at least one occasion,
    2. liver biopsy showing fibrosis
    3. hepatitis B viraemia > 105 copies/ml and/or detectable HbeAg
    • Pegylated interferon should be started first whether the patient is e antigen positive or e antigen negative, and
    o if there is lack of response, consider adefovir or lamivudine
    • Adefovir is preferred over lamivudine due to its low resistance rate
    Treatment of Chronic hepatitis B + cirrhosis + Ascitis
    • HBeAg negative
    o If there is active hepatitis B (ie any detectable DNA in blood) requires treatment by viral suppression.
    o Lamivudine safe and effective drug for the suppression of hepatitis B virus,, Resistance occurs in 15% of patients at 1 year and 60% at 4 years. Adefovir is licensed for second line treatment of Lamivudine resistant HBV.
    • HBeAg positive
    o Antiviral + Interferon , but Interferon is contraindicated in patients with decompensated liver disease,,, The appearance of ascites in a patient with cirrhosis indicates decompensation of their liver disease
    • Liver transplantation is effective in end stage liver disease caused by hepatitis B but adequate viral suppression is the initial treatment of choice pending assessment of suitability for transplantation.

    Hepatitis C
    • degree of activity is determined by the
    o hepatitis C RNA level determined by PCR.
    o This is usually positive within one to two weeks of exposure.
    • Treatment for acute hepatitis is usually only supportive.
    • The treatment for chronic hepatitis C depends on
     the genotype; Those with genotype 2 or 3 can achieve a sustained response after 24 weeks. In genotype 1 and 4, antiviral is continued for 48 weeks due to lower response rates.
     liver histology generally only indicated in those with genotype 1 and 4, as treatment is longer
     RNA level
     clinical presentation.
    o The goal is to identify as early as possible the patients who may respond to the treatment.
    o This is in the form of oral ribavirin and subcutaneous interferon alpha.
    • The transaminase levels bears no correlation with disease severity and often goes up and down over time
    Hepatitis C and pregnancy
    • About 5% infants born to HCV infected women become infected.
    • This occurs at the time of birth and there is no way of preventing this
    • Elective Caesarean section does Not reduce the risk of transmission
    • Factors associated with increase infant infection
    o high viral load at delivery increases the risk of transmission
    o co-infection with HIV increase the risk of transmission.
    o There is no evidence that breast-feeding increases the risk of transmission, but mothers with cracked or bleeding nipples are advised to formula-feed until they are better.
    • Ribavirin is teratogenic
    • There is no vaccine for hepatitis C children under 1 year
    • as there is transmission of the antibodies from the mother they may test positive in the first year "anti hepatitis c" even they have NO active disease
    Intrahepatic cholestasis of pregnancy
    • Symptoms
    o Itching of palms and soles, is the commonest symptom
    o Mild jaundice is seen in 50% of patients,
    o epigastric pain,
    o anorexia, malaise
    o NO nausea NO vomiting
    o bleeding tendency.
    o NO constitutional symptoms
    • Liver function tests
    o cholestatic picture,
    o high alkaline phosphatase (>4× normal)
    o modest elevations in aspartate transaminase (<300 IU/l)
    o bilirubin (<100 µmol/l).
    o prolonged prothrombin time.
    o serum bile acid increased
    o Normal albumin "so exclude acute fatty liver of pregnancy"
    o Normal platelete "so exclude HELLP syndrome"
    • There is an increased
     risk of fetal distress,
     preterm labour and
     perinatal death,
    o therefore careful fetal monitoring is essential.
    • Management includes
    o ursodeoxycholic acid
    o cholestyramine for itch,
    o sometimes vitamin K if there is deranged clotting.
    • Prognosis is excellent for the mother, with symptoms resolving within 2–4 weeks of delivery.
    • It will recur in 40% cases.
    Fatty liver of pregnancy
    • Presentation
    o nausea and vomiting
    o pain in the epigastrium or right upper quadrant
    o Encephalopathy
    o Ascites
    o gestational age 28–42 week range.
    • Investigations
    o Ultrasound is the best imaging modality and allows other conditions such as cholecystitis to be excluded
    o Abnormal investigations include
     hypoglycaemia,
     raised ammonia levels,
     elevated aminotransferase levels,
     elevated white cell count,
     low albumin and
     disseminated intravascular coagulation in up to 75%.
    • Treatment
    o Delivery of the fetus Spontaneous resolution of the condition usually follows delivery.
    o iv fluids and glucose,
    o correction of coagulopathy with fresh-frozen plasma,
    o reduction of exogenous ammonia intake through protein restriction or dietary laxatives to speed evacuation of nitrogenous wastes


    Pre-eclampsia
    • Presentation
    o severe headache, BP is 140/90 mmHg
    o peripheral oedema,
    o indigestion
    o proteinuria
    o Eclampsia is above + seizures
    • Investigations
    o Microangiopathic haemolytic anaemia,
    Hb 9.0 g/dl
    WCC 7.1 x109/l
    PLT 68 x109/l
    Creatinine 185 μmol/l
    AST 205 U/l
    ALT 150 U/l
    ALP 301 U/l
    Bilirubin 80 μmol/l
    Urine protein ++
    • Treatment
    o control of blood pressure
    o rapid assessment of the pregnancy by the obstetric team.
    o delivery of the child
    Child Pugh score
    • based on
     bilirubin,
     albumin,
     prothrombin time,
     ascites
     encephalopathy.
    • Grade A predicts a life expectancy about 15–20 years with a 10% abdominal peri-operative mortality.
    • Grade C predicts life expectancy about 1–3 years and an 80% per-op mortality.
    • Grade B indicates transplantation consideration with a 30% per-operative mortality.
    • A serum sodium less than 110 mmol/l also carries a poor prognosis.

    Cirrhosis may result in falsely elevated levels of CA-125.

    Budd Chiari syndrome
    • Presentation "It can present either acutely or chronically"
    o Acute
     abdominal pain,
     hepatomegaly,
     jaundice
     sometimes fulminant hepatic failure
    o Chronic
     signs of cirrhosis and
     portal hypertension
    • Causes
    o primary polycythaemia,
    o leukaemia
    o oral contraceptive pill
    o thombophilias as
    • "antiphospholipid syndrome"
    o Renal failure
    o The prolonged APTT
    o normal PT is suggestive of lupus anticoagulant.
    o Other causes include malignancy (especially hepatocellular, renal and adrenal), radiotherapy
    • Investigation
    o Ascitic fluid analysis will show a high protein content
    o Colour flow Doppler ultrasound of the hepatic vasculature show obliteration of the hepatic veins
    o Liver biopsy usually shows centrilobular congestion with fibrosis
    • Treatment is with
    o Control of the ascites and
    o Treatment with streptokinase and subsequent anticoagulation may be attempted if the thrombus is known to be of recent onset
    o Liver transplantation is the only option in the acute presentation, which has a very poor prognosis, with two-thirds of patients dead within 1 year

    Liver cirrhosis with varices
    • Propranalol is potentially most effective in reducing progression of cirrhosis.
    • Management of acute hemorrhage
    o Fresh-frozen plasma should be used for the coagulopathy, which could be made worse by repeated blood transfusions. Vitamin K should also be given, but will not work immediately.
    • Procedures for controlling bleeding
    o Combination of banding + terlipressin appears to be most effective in
     controlling acute variceal bleed,
     rebleeding rate and
     early complications.
    o Combination of Sclerotherapy + terlipressin as a second choice if banding is not possible for technical reasons
    o Sclerotherapy is superior to
     balloon tamponade alone,
     terlipressin alone and
     a combination of terlipressin and balloon tamponade
    o terlipressin , Somatostatin, octreotide is effective in acute management of variceal bleed, but combined therapy has been shown to be more effective.
    o Terlipressin is more effective than octreotide, but it is contraindicated in ischaemic heart disease
    o Sengstaken tube is an effective, until endoscopy can be performed
    o After endoscopic therapy, 50% of patients will re-bleed within 10 days and up to 80% re-bleed over a 2-year period.
    o Mortality of variceal bleed is 50% with each episode.
    o Transjugular intrahepatic portosystemic shunt (TIPPS) can be used in cases where haemorrhage cannot be stopped with two sessions of endoscopic therapy over 5 days.
    o Surgery is occasionally performed
    o According to the British Society of Gastroenterology guidelines, patients with grade 2 or 3 varices on elective endoscopy require propranolol prophylaxis
    Spontaneous bacterial peritonitis
    • Presentation
    o History of chronic liver disease
    o worsening of jaundice with a rising bilirubin and increasing ascites and increasingly drowsy,,, features like encephalopathy
    o Pain and pyrexia may frequently be absent
    • occurs in around 8% of cirrhotic
    • A raised neutrophil count alone in ascitic fluid is enough to commence treatment.
    • Mortality is high at up to 25% and recurs in 70% of patients within one year.

    Primary biliary cirrhosis
    • Lethargy and pruritus are the usual first symptoms before jaundice
    • Once jaundice develops survival is less than 2 years
    • Associated with other autoimmune conditions
    o Sjögren’s syndrome,
    o scleroderma,
    o CREST
    o SLE.
    o membranous glomerulonephritis and
    o renal tubular acidosis
    • Common serum abnormalities at presentation include
    o raised alkaline phosphatase, and GGT
    o mildly elevated transaminases
    o elevated serum lipids.
    o antimitochondrial antibodies (in 90–95% of cases)
    o The presence of anti-mitochondrial antibody of a titre > 1:40 is highly suggestive of PBC
    • Imaging important to exclude biliary obstruction
    o Abdominal US "first choice"
    o Abdominal CT scan
    o MRCP
    • Treatment
    o in early disease, high dose ursodeoxycholic acid is well tolerated, improves liver biochemistry and may slow disease progression.
    o Liver transplantation is an option for end stage disease, where the
     development of portal hypertension,
     jaundice and hepatocellular failure
     bilirubin greater than 100 µmol/l.
     Intractable pruritus
    o The 5-year survival post transplant is about 70–80%.

    Hereditary haemochromatosis
    • HFE gene on chromosome 6
    • Genetic screening for homozygous C282Y or H63D mutations
    • Cardiac and liver damage may improve with treatment but joint pain and diabetes often remain.

    Wilson disease
    • Ataxia and tremor are common
    • In Fulminant W.D. there is massive hepatic necrosis releasing the abnormally sequestered copper from the hepatocytes into the circulation leading to haemolysis and increased serum copper
    • Kayser Fleischer rings on the cornea are the most specific sign although they may be absent in up to 50% of cases.
    • Serum caeruloplasmin is low, but is sometimes normal and can also be reduced by advanced liver failure from any cause, so it is a non-specific test.
    • Urinary copper excretion is increased
    • The diagnosis can also be made by liver biopsy
    • Genetic testing is unhelpful in most cases unless there is a strong family history, as there are 200 mutations in the gene known
    Autoimmune hepatitis.
    • Treatment
    o an initial period of high-dose prednisolone,
    o azathioprine is often added as a steroid-sparing agent
    • Confirming diagnosis
    o Liver biopsy is the investigation most likely to confirm the diagnosis
    o Generally in these cases imaging is unhelpful
    Hydatid liver disease
    • Calcification is often seen on plain abdominal X-ray.
    • Ultrasound is demonstrate cysts
    • CT is occasionally used when the character of the cysts is unclear.
    • Serology is neither specific nor sensitive.
    • Treatment
    o high dose albendazole of 10 mg/kg is given for 1-3 months followed by percutaneous aspiration and sterilisation with alcohol.
    o Percutaneous aspiration on its own is contraindicated as toxins can be released causing cardiovascular collapse.
    o Surgery
    Amoebic liver abscess
    • Presentation
    o without bowel changes in up to 50% of cases.
    o high swinging fever
    o right upper quadrant pain
    o raised right hemidiaphragm and dullness on examination.
    • Investigation
    o Ultrasound or CT abdomen first choice
    o Stool examination although this test has limitations in terms of sensitivity
    o Stool antigen detection may be helpful and facilitates early diagnosis before an antibody response occurs (<7 d) and differentiates pathogenic from nonpathogenic Entamoeba infection
    o Serology " Indirect haemagglutination test" is positive in greater than 95% but this could be past or present infection.
    • Treatment
    o Metronidazole is the first line treatment for the amoebic dysentery, and diloxanide is used to destroy the cysts.
    o Abscess drainage is only needed if
     concerned about a mass rupture as it can spread into the lung or
     if there is no response to oral treatments.

    Hepatic adenoma caused by oral contraceptive pill
    • Stop the oral contraceptive pill
    • Patients who experience some regression after stopping the pill, there is still a risk of malignant transformation, and then arrange
    • later surgical resection
    • if Patients are unwilling/unable to undergo elective tumour resection, such patients should be monitored with alpha-fetoprotein measurement
    Hepatocellular carcinoma
    • Diagnosis
    o Ultrasound and CT scan
    o A rising alpha-fetoprotein indicative of a hepatoma and
    o biopsy is not always necessary to avoid seeding of tumour
    • Surgical Treatment is the only proven potentially curative therapy
    o Hepatic resection should be considered as a primary therapy in any patient with non-cirrhotic liver.
    o liver transplantation in any cirrhotic patient with
     cirrhosis and a single small HCC (<5 cm) or
     cirrhosis and up to three lesions (<3 cm).
    • Non-surgical therapy is only used when
    • surgical therapy is not possible and
    • with extrahepatic dissemination.
    o Percutaneous ethanol injection has been shown to produce necrosis of small HCC and is best suited for peripheral lesions.
    o Chemoembolisation can produce tumour necrosis and has been shown to affect survival in highly selected patients with good liver reserve.
    o Systemic chemotherapy has a poor response rate and
    o hormonal therapy like tamoxifen has shown no survival benefit in controlled trials.
    o Interferon has been used for treatment of HCC rather than the underlying viral infection, but remains controversial.
    Acute graft-versus host-disease after liver transplantation
    • It develops from 15 days after transplantation
    • Presentation is with
    o jaundice,
    o hepatomegaly and
    o abnormal liver function tests, the earliest and most common finding being a rise in the serum levels of
    • conjugated bilirubin and
    • alkaline phosphatase.
    • This reflects damage to the bile canaliculi, leading to cholestasis.
    • Other disorders need to be excluded, such as
    o hepatic veno-occlusive disease,
    o hepatic infections (primarily viral hepatitis) and
    o drug toxicity.
    • A biopsy gives definite histological diagnosis
    o A transjugular hepatic biopsy may be preferred if an adequate amount of tissue can be obtained.
    o The primary histologic finding is
    • extensive bile duct damage
    • Treatment
    o the first and most effective treatment option is the use of corticosteroids "methylprednisolone".
    o If higher doses of steroids are not successful in controlling GVHD by 3 to 5 days, second-line treatments are less successful. These include
    • cyclosporine,
    • tacrolimus,
    • antithymocyte globulin, and
    • mycophenolate mofetil.
    Kings criteria for liver transplant include:
    1) > 1 week between onset of jaundice and encephalopathy
    2) Bilirubin > 300 μmol/l
    3) PT > 50
    4) Drug induced liver failure
    5) Age <10 or >40

    Patient has to meet 3/5 of the above OR
    PT > 100
    Long-term prophylaxis with hepatitis B immunoglobulin is associated with a significant lower risk of re-infection post transplant. Alternatives include use of nucleoside analogues such as famciclovir and lamivudine.
    Primary sclerosing cholangitis
    • Jaundice tends to fluctuate in primary sclerosing cholangitis, unlike primary biliary cirrhosis, which is progressive
    • If associated with ulcerative colitis,, Colectomy has no effect on the natural history of PSC development at all.
    • Ultrasound is normal in 50% of patients at an early stage of disease.
    • MRCP has an accuracy of diagnosis for PSC of 90%, compared to 97% for ERCP but with a much better safety profile. In addition, MRCP gives the possibility of visualising bile ducts proximal to any obstruction.
    • Liver transplantation is best choice
    • Survival post liver transplant however is around 90%, although the chance of rejection is higher in PSC patients.
    • 10-15% of PSC patients eventually develop cholangiocarcinoma.
    • cholangiocarcinoma to be a contraindication to liver transplantation
    • When cholangiocarcinoma with local invasion occur, the treatment of choice is stenting via ERCP. The procedure is successful at relieving symptoms of jaundice

    Sphincter of Oddi dysmotility (SOD)
    • can cause backup of bile and pancreatic juices which can result in biliary colic. recurrent admissions for intermittent upper abdominal pain especially after fatty
    • More prolonged obstruction may result in bile leaking back into the bloodstream, which can cause transient abnormal liver biochemistry.
    • SOD most commonly occurs in young females especially those who have previously undergone cholecystectomy.
    • At ERCP, delayed drainage of contrast is seen and
    • SOD manometry can confirm the diagnosis,,,There is usually a high resting pressure with marked phasic contractions and often some retrograde peristalsis.
    • Endoscopic sphincterotomy or balloon sphincteroplasty often relieves this condition
    Ascending cholangitis
    • In the acute setting
    o the most important first steps in management are to
     exclude bowel perforation erect chest X ray
     evaluate the degree of metabolic compromise due to sepsis/shock (arterial blood gas, ABG) to
    • Subsequent acute management would include an
    o abdominal ultrasound for any biliary dilatation, which may be a precursor to
    o urgent ERCP
    o Blood cultures should also be taken prior to commencing antibiotics, but should not delay their administration.
    o Ultrasonography is excellent for
     gallstones and cholecystitis.
     assessing bile duct dilatation.
     However, it often misses stones in the distal bile duct
    o ERCP is both diagnostic and therapeutic and is considered the criterion standard for imaging the biliary system.
     ERCP should be reserved for patients who may require therapeutic intervention.
     Patients with a high clinical suspicion for cholangitis should proceed directly to ERCP.
     ERCP has a high success rate (98%) and is considered safer than surgical and percutaneous intervention.
     Diagnostic use of ERCP carries a complication rate of approximately 1.38% The major complication nclude pancreatitis, bleeding, and perforation.
    o For diagnostic purposes, ERCP has now generally been replaced by MRCP
    o MRCP is a noninvasive imaging modality that is increasingly being used in the diagnosis of biliary stones and other biliary pathology.
     MRCP is accurate for detecting choledocholithiasis, neoplasms, strictures, and dilations within the biliary system.
     Limitations of MRCP include the inability for invasive diagnostic tests such as bile sampling, cytologic testing, stone removal, or stenting.
     It has limited sensitivity for small stones (<6 mm in diameter).
     Absolute contraindications are the same as for a traditional MRI, which include the
    • presence of a cardiac pacemaker,
    • cerebral aneurysm clips,
    • ocular or cochlear implants, and
    • ocular foreign bodies.
     Relative contraindications include the
    • presence of cardiac prosthetic valves,
    • neurostimulators,
    • metal prostheses, and
    • penile implants.



    Carcinoid syndrome
    • Diagnosis Carcinoid Tumor
    o chest and abdominal computed tomography (CT)
    o pentreotide imaging has been shown to have a sensitivity of 80%+ for detection of carcinoid.
    • Diagnosis Carcinoid syndrome
    o 24-h urine collection for 5-HIAA
    o Liver ultrasonography to visualise the liver metastases.
    • Management of the carcinoid syndrome is largely palliative and involves
    o Reducing the tumour mass by a combination of surgical resection, hepatic artery embolisation and,
    o Rarely, cytotoxic chemotherapy.
    o The effects of the tumour products can be inhibited
    • octreotide or
    • cyproheptadine.
    Investigations for iron deficiency anaemia in elderly
    • Any level of anaemia with evidence of iron deficiency (i.e. microcytosis, hypochromasia or low serum ferritin) should be investigated.
    • upper and lower gastrointestinal (GI) tract to exclude malignancy.
    • There is no evidence of the benefit of colonoscopy over good contrast studies for the detection of GI cancer and therefore either is acceptable.
    • Coeliac disease is estimated to account for up to 6% of total cases of IDA, and this can sometimes occur in the presence of normal B12 and folate levels.
    o anti-endomysial antibody or
    o tissue transglutaminase antibody) with
    o duodenal biopsy used to confirm positive results or to make a diagnosis in serologogy-negative patients in whom coeliac disease is strongly suspected e.g. those with
    • selective immunoglobulin A (IgA) deficiency or
    • with a strong family history)
    • Urinary testing for blood is recommended as an estimated 1% of patients with IDA will have renal tract malignancy caused by haematuria and haemosiderin deposition in the tumour.
    • Faecal occult blood testing is of no benefit in the investigation of established IDA as it is insensitive and non-specific, although it may have a role in population screening for GI cancer.
    Iron deficiency anaemia In women aged less than 50 years who menstruate regularly
    • Menstrual blood loss is a common cause of IDA
    • For this reason it is recommended that in the absence of warning features in the personal medical history or family history, or on examination, that a trial of ferrous sulphate and 3-month review , and
    • Only those patients who remain anaemic after an appropriate interval (or who are transfusion dependent) are investigated further.
    • Pre-menopausal women who have IDA and a strong family history of colorectal cancer should be investigated immediately
    • British Society of Gastroenterology guidelines state that a strong family history consists of one first-degree relative affected aged <45 years, or two affected first-degree relatives
    Pellagra
    • dermatitis, depression and dementia.
    • tremor, ataxia, insomnia, fits and neuropathy.
    • It most commonly presents in
    o China and Africa and
    o side-effect of tuberculosis (TB) treatment
    o carcinoid syndrome.

    Drugs causing chronic diarrhoea include
    • broad-spectrum antibiotics,
    • antihypertensives such as diuretics,
    • digoxin,
    • Lansoprazole
    • Fluoxetine
    • cholesterol lowering drugs,
    • sodium valproate,
    • thyroxine,
    • levodopa,
    • antacids,
    • theophylline,
    • colchicines and
    • oral hypoglycaemic drugs.

    Diagnostic paracentesis
    • serum to ascites albumin gradient
    o ascites related to portal hypertension (gradient > 11g/L) increased
     cirrhosis,
     alcoholic hepatitis,
     schistosomiasis,
     fulminant hepatic failure,
     Budd Chiari syndrome,
     acute or chronic portal vein obstruction,
     cardiac diseases
     spontaneous bacterial peritonitis secondary to cirrhosis.
    o ascites not related to portal hypertension (gradient < 11g/L).decreased
     nephrotic syndrome,
     protein losing enteropathy,
     peritoneal carcinomatosis,
     tuberculous peritonitis,
     pancreatic duct leak and biliary ascites.
  43. drjim

    drjim Guest

    @score ............kerala....
  44. drjim

    drjim Guest

    @score ....where r u from?
  45. sarahpart2

    sarahpart2 Guest

    awaiting more plz dr albarawi
  46. Dr Oman - thank you for your interest. I was also lucky enough to pass alhamdulillah. Very many congratulations to you, Dr Albawari, sarahmrcp2 and everyone who contributed to the forum.

    To anyone who failed I know exactly how that feels, but it makes victory sweeter ultimately. I have every faith that you will pass this cruel exam eventually.

    I studied Pastest (religiously) and found the interactive videos extremely helpful plus this helped me to stop falling asleep during the long hours of revision. Try to finish the site at least once.

    I found every book I could by Huw Beynon, BOF or otherwise and read and re-read them - the explanations are fantastic.

    Also look at the free questions available on the MRCP uk site - the format and tone of some of the questions was very familiar to the questions that appeared in the April exam.

    Do not touch onexam - this mistake cost me dearly in the past. Lots of wrong answers on there and misleading explanations.

    Know EVERYTHING about HIV before you enter the exam hall and the RCP remain obsessed with the thyroid, amiodarone and know ALL your ECGs backwards.

    Sharma's book was also useful.

    I cannot learn by taking notes but I'm sure if you do that might also help.

    And now PACES...
  47. abcde

    abcde Guest

    Please, please, please give me an advice

    Will somebody with 66% at onexamination and 63% at Pastest pass this tricky MRCP Part 2 exam?

    I have heard many stories about how difficult the exam is. I won't be able to study anymore as I have a very packed schedule from now onwards. Definitely won't be able to study anymore.

    Should I apply for July exam? Or should I wait until November?
    The exam is very expensive. I really hope I can pass.

    I know there are a lot of nice people in this forum.

    What do you think?


    Dr Albarwari, what do you think?

    Dr Oman, what do you think?

    Dr velocity_girl, what do you think?

    Dr jim, what do you think?

    Dr sarahpart2, what do you think?

  48. con

    con Guest

    @abcde. The exam is difficult but you only need ~55% to pass. since there is no negative marking, you would get 20% with random guessing. Therefore you only need to get ~35/80 =~ 45% to pass.
    You'd do well to listen to the advice given above and avoid onexamination!
  49. sarahpart2

    sarahpart2 Guest

    avoid onexamination at all cost , lost of wrong answers

    go for novemebr , july too close
  50. Drcool

    Drcool Guest

    Sarahpart2.. What are your plans for paces?

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